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7/31/2019 Project Paediatric
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Topic:
INCIDENCE AND MANAGEMENT OUTCOME OF BRONCHOPNEUMONIA IN CHILDREN (1-5 yrs.) IN UPTH
Abstract
AIM: Poorly treated bronchopneumonia is the most common cause of
empyema thoracis in Nigeria. Ignorance poverty and quackery are the
major reasons for inadequate treatment.
METHOD: All paediatric patients diagnosed treated for
bronchopneumonia in our hospital between November 2010 and
December 2009 had their case notes retrieved, and data collated into
individual proforma for analysis.
RESULTS: During the 26 months period, there were 2106 admissions
into children emergency unit of our hospital, with 267 havingbronchopneumonia (12%) and 18 having empyema thoracis (6.7% case
prevalence). The age range was 1 month to 16 years with mean of 6.4
years and male: female ratio 3.5: 1. The right pleural space was affected
in 50%, left pleural space in 33.33%, and both pleural spaces in 16.66%.
Up to 61% of mothers of the patients with empyema thoracis had no or
only primary level of formal education, 77.78% of such mothers were
not gainfully employed and 44.43% of patients were previously treated
by medical charlatans before presentation in our hospital. All patientswere successfully treated with antibiotic and tube thoracostomy drainage
with satisfactory recovery.
CONCLUSION: Bronchopneumonia is still prevalent in Nigeria. Mass
literacy campaign, poverty alleviation and provision of affordable and
easily accessible medical care throughout the whole country are the
immediate solution to this menace.
Key words: Bronchopneumonia
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INTRODUCTION
Bronchopneumonia is an inflammation of the lungs caused by bacteria in which
the air sacs (alveoli) become filled with inflammatory cells which has a
characteristic shadow widespread. This infection usually starts in a number of
small bronchi and spread in a patchy manner into the alveoli (Oxford Medical
Dictionary, 2003).
Pneumonia and other lower respiratory tract infections are the leading causes of
death worldwide. Because pneumonia is common and is associated with significant
morbidity and mortality, properly diagnosing pneumonia, correctly recognizing
any complications or underlying conditions, and appropriately treating patients are
important. Although in developed countries the diagnosis is usually made on the
basis of radiographic findings, the World Health Organization (WHO) has defined
pneumonia solely on the basis of clinical findings obtained by visual inspection
and on timing of the respiratory rate.
Pneumonia may originate in the lung or may be a focal complication of a
contiguous or systemic inflammatory process. Abnormalities of airway patency as
well as alveolar ventilation and perfusion occur frequently due to various
mechanisms. These derangements often significantly alter gas exchange and
dependent cellular metabolism in the many tissues and organs that determine
survival and contribute to quality of life. It is on this background that the disease
assumes alarming proportion if both the lungs are affected. Great care has to be
taken if the patient suffers from bronchopneumonia because if left untreated the
outcome may be fatal.
Recognition, prevention, and treatment of these problems are major factors in the
care of children with pneumonia.
Pathogenesis
Pneumonia is characterized by inflammation of the alveoli and terminal airspaces
in response to invasion by an infectious agent introduced into the lungs through
hematogenous spread or inhalation. The inflammatory cascade triggers the leakage
of plasma and the loss of surfactant, resulting in air loss and consolidation.
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INCIDENCE AND MANAGEMENT OUTCOME OF BRONCHOPNEUMONIA IN CHILDREN (1-5 yrs.) IN UPTH
The activated inflammatory response often results in targeted migration of
phagocytes, with the release of toxic substances from granules and other
microbicidal packages and the initiation of poorly regulated cascades (eg,
complement, coagulation, cytokines). These cascades may directly injure hosttissues and adversely alter endothelial and epithelial integrity, vasomotor tone,
intravascular hemostasis, and the activation state of fixed and migratory
phagocytes at the inflammatory focus. The role of apoptosis (noninflammatory
programmed cell death) in pneumonia is poorly understood.
Pulmonary injuries are caused directly and/or indirectly by invading
microorganisms or foreign material and by poorly targeted or inappropriate
responses by the host defense system that may damage healthy host tissues as
badly or worse than the invading agent. Direct injury by the invading agent usuallyresults from synthesis and secretion of microbial enzymes, proteins, toxic lipids,
and toxins that disrupt host cell membranes, metabolic machinery, and the
extracellular matrix that usually inhibits microbial migration.
Indirect injury is mediated by structural or secreted molecules, such as endotoxin,
leukocidin, and toxic shock syndrome toxin-1 (TSST-1), which may alter local
vasomotor tone and integrity, change the characteristics of the tissue perfusate, and
generally interfere with the delivery of oxygen and nutrients and removal of waste
products from local tissues.(Barnett, Klein. 2006; Bone, Grodzin, Balk. 1997)
On a macroscopic level, the invading agents and the host defenses both tend to
increase airway smooth muscle tone and resistance, mucus secretion, and the
presence of inflammatory cells and debris in these secretions. These materials may
further increase airway resistance and obstruct the airways, partially or totally,
causing airtrapping, atelectasis, and ventilatory dead space. In addition, disruption
of endothelial and alveolar epithelial integrity may allow surfactant to be
inactivated by proteinaceous exudate, a process that may be exacerbated further by
the direct effects of meconium or pathogenic microorganisms.
In the end, conducting airways offer much more resistance and may becomeobstructed, alveoli may be atelectatic or hyperexpanded, alveolar perfusion may be
markedly altered, and multiple tissues and cell populations in the lung and
elsewhere sustain injury that increases the basal requirements for oxygen uptake
and excretory gas removal at a time when the lungs are less able to accomplish
these tasks.
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Alveolar diffusion barriers may increase, intrapulmonary shunts may worsen, and
ventilation/perfusion (V/Q) mismatch may further impair gas exchange despite
endogenous homeostatic attempts to improve matching by regional airway and
vascular constriction or dilatation. Because the myocardium has to work harder toovercome the alterations in pulmonary vascular resistances that accompany the
above changes of pneumonia, the lungs may be less able to add oxygen and
remove carbon dioxide from mixed venous blood for delivery to end organs. The
spread of infection or inflammatory response, either systemically or to other focalsites, further exacerbates the situation.
Viral infections are characterized by the accumulation of mononuclear cells in the
submucosa and perivascular space, resulting in partial obstruction of the airway.
Patients with these infections present with wheezing and crackles (see ClinicalPresentation). Disease progresses when the alveolar type II cells lose their
structural integrity and surfactant production is diminished, a hyaline membrane
forms, and pulmonary edema develops.
In bacterial infections, the alveoli fill with proteinaceous fluid, which triggers a
brisk influx of red blood cells (RBCs) and polymorphonuclear (PMN) cells (red
hepatization) followed by the deposition of fibrin and the degradation of
inflammatory cells (gray hepatization). During resolution, intra-alveolar debris is
ingested and removed by the alveolar macrophages. This consolidation leads to
decreased air entry and dullness to percussion; inflammation in the small airwaysleads to crackles (see Clinical Presentation).
Four stages of lobar pneumonia have been described. In the first stage, which
occurs within 24 hours of infection, the lung is characterized microscopically by
vascular congestion and alveolar edema. Many bacteria and few neutrophils are
present. The stage of red hepatization (2-3 days), is so called because of its
similarity to the consistency of liver, which is characterized by the presence of
many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin within the
alveoli. In the stage of gray hepatization (2-3 d), the lung is gray-brown to yellow
because of fibrinopurulent exudate, disintegration of RBCs, and hemosiderin. The
final stage of resolution is characterized by resorption and restoration of the
pulmonary architecture. Fibrinous inflammation may lead to resolution or to
organization and pleural adhesions.
Bronchopneumonia, a patchy consolidation involving one or more lobes, usually
involves the dependent lung zones, a pattern attributable to aspiration of
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INCIDENCE AND MANAGEMENT OUTCOME OF BRONCHOPNEUMONIA IN CHILDREN (1-5 yrs.) IN UPTH
oropharyngeal contents. The neutrophilic exudate is centered in bronchi and
bronchioles, with centrifugal spread to the adjacent alveoli.
In interstitial pneumonia, patchy or diffuse inflammation involving the interstitiumis characterized by infiltration of lymphocytes and macrophages. The alveoli do
not contain a significant exudate, but protein-rich hyaline membranes similar to
those found in adult respiratory distress syndrome (ARDS) may line the alveolar
spaces. Bacterial superinfection of viral pneumonia can also produce a mixedpattern of interstitial and alveolar airspace inflammation.
Miliary pneumonia is a term applied to multiple, discrete lesions resulting from the
spread of the pathogen to the lungs via the bloodstream. The varying degrees of
immunocompromise in miliary tuberculosis (TB), histoplasmosis, and
coccidioidomycosis may manifest as granulomas with caseous necrosis to foci of
necrosis. Miliary herpesvirus, cytomegalovirus (CMV), or varicella-zoster virus
infection in severely immunocompromised patients results in numerous acute
necrotizing hemorrhagic lesions.
Background to the Problem
In the cause of my nursing care to patients in the paediatric unit (Children Medical
Ward) in University of Port Harcourt teaching hospital, I observered several cases
of bronchopneumonia among children (1-5 years). Seasonal fluctuations on theincidence (per month) were also noticed. All these motivated me towards having
in-depth knowledge of the disease.
In my quest to know the incidence rate and the management outcome, I also
observed co-relationship between the mothers knowledge base and the prognosisof the disease.
Statement of the problem
Despite the health education given to mothers in their Ante-Natal and Post-Natalroutine health visit about healthy living environment, good nutrition, shelter, safe
drinking water and possible risk factors to childhood disease, it was observed that
minimal percentage of mothers implements them as evidenced by an increase rate
of admission into the Children Medical Ward for a diagnosis of Pneumoniaespecially bronchopneumonia.
http://emedicine.medscape.com/article/221777-overviewhttp://emedicine.medscape.com/article/1002185-overviewhttp://emedicine.medscape.com/article/781632-overviewhttp://emedicine.medscape.com/article/781632-overviewhttp://emedicine.medscape.com/article/1002185-overviewhttp://emedicine.medscape.com/article/221777-overview -
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INCIDENCE AND MANAGEMENT OUTCOME OF BRONCHOPNEUMONIA IN CHILDREN (1-5 yrs.) IN UPTH
Purpose of study
This study aims at determining the management outcome of patients (children 1-5
years) diagnosed with bronchopneumonia in UPTH.
Specific Objectives of the study
To determine the number of children (1-5 years) admitted with bronchopneumoniawithin 2009-2011.
To determine the management outcome bronchopneumonia of children (1-5 years)in UPTH.
To determine the childrens (patient) parent educational status
To determine the economic status of my patients family.
Research questions
1. What is the incident rate of bronchopneumonia cases admitted within 2009-2011 in children medical ward?
2. What is the management outcome of bronchopneumonia of children (1-5years) in UPTH?
3. What is the educational status of Parents whose children are diagnosed ofbronchopneumonia?
4. What is the economic status of parents whose children are diagnosed ofbronchopneumonia?
Hypothesis
There is a significant relationship between Economic and Educational status ofparents to bronchopneumonia infection in children (1-5 years).
Scope of study
This study will limit itself to children (1-5 years) admitted into the children
emergency and children medical wards with diagnosis of bronchopneumonia.
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Limitations and Delimitations
The most prominent obstacle encountered in the course of this work was the time
frame.
This was overcome by educating and mobilizing friends who aided me in retrieval
of trivial information from my subjects medical record.
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INCIDENCE AND MANAGEMENT OUTCOME OF BRONCHOPNEUMONIA IN CHILDREN (1-5 yrs.) IN UPTH
LITERATURE REVIEW
Incidence of clinical pneumonia
Rudan et al (2004) calculated and published the first global estimate of the
incidence of clinical pneumonia in children aged less than 5 years for the year
2000. This estimate was based on the analysis of data from selected 28
community-based longitudinal studies done in developing countries that were
published between 1969 and 1999. These studies were the only sources meeting
the predefined set of minimum-quality criteria for inclusion in the analysis (Rudan,
Tomaskovic, Boschi-Pinto, Campbell; 2004). The estimated median incidence for
developing countries was 0.28 episodes per child-year, with an interquartile range
0.210.71 episodes per child-year (Rudan, Tomaskovic, Boschi-Pinto, Campbell; 2004). The
variation in incidence between the selected studies was very large, most probably
due to the distinct study designs and real differences in the prevalence of risk
factors in the various study settings. Given the substantial uncertainty over the
point estimate, we used a triangular approach to check for plausibility of our
assessment of pneumonia incidence. The ranges obtained by the main appraisal
and two ancillary assessments overlapped between the values of 148 and 161
million new episodes per year. Giving most weight to the estimate obtained
through the main approach, the analyses suggested that the incidence of clinical
pneumonia in children aged less than 5 years in developing countries worldwide
(WHO regions B, D and E; see Annex A) is close to 0.29 episodes per child-year.
This equates to 151.8 million new cases every year, 13.1 million (interquartile
range: 10.619.6 million) or 8.7% (713%) of which are severe enough to require
hospitalization (Rudan, Tomaskovic, Boschi-Pinto, Campbell; 2004). In addition, a further 4
million cases occur in developed countries worldwide (all WHO regions A and
Europe regions B and C). The regions and their populations are defined by WHO
region and child and adult mortality stratum (Table 1 and the statistical annex of
World Health Report 2000, available: at
http://www.who.int/whr2001/2001/archives/2000/en/pdf/Statistical_Annex.pdf)
(World population prospects: population database. United Nations Population Division; 2006. Availablefrom: http://esa.un.org/unpp [accessed on 1 April 2008]).
It is of major public health interest to assess the distribution of these estimated 156
million episodes by regions and countries to assist planning for preventive
interventions and case management at community and facility levels, including
http://www.who.int/whr2001/2001/archives/2000/en/pdf/Statistical_Annex.pdfhttp://www.who.int/whr2001/2001/archives/2000/en/pdf/Statistical_Annex.pdfhttp://esa.un.org/unpphttp://esa.un.org/unpphttp://www.who.int/whr2001/2001/archives/2000/en/pdf/Statistical_Annex.pdf -
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vaccine and antibiotic needs and delivery. Therefore, we calculated these figures
with the model described in Appendix A. Table 2 shows the 15 countries with the
highest predicted number of new pneumonia episodes and their respective
incidence. These 15 countries account for 74% (115.3 million episodes) of theestimated 156 million global episodes. More than half of the worlds annual newpneumonia cases are concentrated in just five countries where 44% of the worldschildren aged less than 5 years live: India (43 million), China (21 million) and
Pakistan (10 million) and in Bangladesh, Indonesia and Nigeria (6 million each).
When the prevalence of exposure was set to 99% (an unrealistic scenario at the
country level, even for the poorest countries of the world) the incidence computed
by the model was about 0.77 episodes per child-year. This estimate is slightly
above the upper limit of individually reported pneumonia incidence from the 28community-based studies from the developing world (75% interquartile range
estimate of 0.71 episodes per child-year). The model yields plausible estimates
over a wide range of values of risk-factor prevalence, supporting its use forcalculating the distribution of clinical pneumonia episodes.
Causes of pneumonia in children
These infections usually arise in the summer and fall and bacteria may be found in
the water condensed from air conditioning systems or in contaminated hospital
water systems.
Although everyone is at risk, adolescents and young adults are most commonly
affected by chlamydial pneumonia.
Childhood clinical pneumonia is caused by a combination of exposure to risk
factors related to the host, the environment and infection. These risk factors for
development of pneumonia, related to the host or the environment, are listed
below:
Definite risk factors
Malnutrition (weight-for-age z-score
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Likely risk factorsParental smoking
Zinc deficiency
Mothers experience as a caregiverConcomitant diseases (e.g. diarrhoea, heart disease, asthma)
Possible risk factorsMothers education
Day-care attendance
Rainfall (humidity)
High altitude (cold air)
Vitamin A deficiency
Birth order
Outdoor air pollution
Before vaccines were available, the cause of childhood pneumonia was a matter of
great interest as specific therapy was available for pneumococcal pneumonia of
certain serotypes, requiring not only an etiological diagnosis for effective therapy,
but also pneumococcal serotyping. Studies from that era identified Streptococcus
pneumoniae (pneumococcus) andHaemophilus influenzae as the main bacterial
causes of pneumonia, with some severe cases caused by Staphylococcus aureus
and Klebsiella pneumonia(Shann; 2006). In the modern era, our understanding of the
causes of pneumonia in developing countries is based on two types of study. The
first type consists of prospective hospital-based studies that have relied on bloodcultures and, in some studies, of percutaneous lung aspiration (Adegbola et al.; 1994).
Some other studies also examined nasopharyngeal specimens for virus
identification (Weber; Mulholland; Greenwood; 1998). This approach lacks sensitivity
for the identification of bacterial cause. Attempts to augment culture-based
methods with various indirect markers of bacterial cause have been largely
unsuccessful as the tests employed have been unable to distinguish between
carriage of pneumococcus andH. influenzae, which is usual for children in
developing countries, and invasive disease (Goldblatt; Miller; McCloskey; Cartwright;
1998). The second type of study is the vaccine trial, in which the burden ofpneumonia prevented by a specific vaccine is presumed to be a minimum estimate
of the burden of pneumonia due to the organism against which the vaccine isdirected (Mulholland; 2004).
In prospective microbiology-based studies, the leading bacterial cause is
pneumococcus, being identified in 3050% of pneumonia cases (Shann; 2006,
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Adegbola; et al. 1994, Forgie; et al. 1991, Forgie; et al. 1991, Kamiya et al 1997, Falade; Mulhollan;
Adegbo; Greenwood; 1997).The second most common organism isolated in most
studies is H. influenzae type b (Hib; 1030% of cases), followed by S. aureus and K.
pneumoniae. In addition, lung aspirate studies have identified a significantfraction of acute pneumonia cases to be due to Mycobacterium tuberculosis,
which is notoriously difficult to identify in children (Falade; et al. 1997). Controversy
surrounds the role of three important organisms, non-typableH. influenzae
(NTHI), S. aureus and non-typhoid Salmonella spp. NTHI was found to be an
important pathogen in a lung aspirate study from Papua New Guinea (Shann; et al.
2004), whereas in a series of lung aspirate studies from the Gambia, and in most
blood culture-based studies, Hib was the main type ofH. influenzae identified
(Adegbola; et al. 1994). Studies from Pakistan found NTHI to be a common blood
culture isolate (Straus; et al., 1998), but this has not been replicated elsewhere. The
first major study of the modern era that used lung aspiration on over 500 children
in Chile, including normal controls, foundS. aureus to be the main pathogen. This
finding has not been replicated in more recent studies, although a recently
completed WHO study of very severe (hypoxaemic) pneumonia in seven countries
found S. aureus in 47 of the 112 cases (42% of cases) in which a bacterium was
identified, making it the second largest cause (Asghar; et al., 2008). The role of non-
typhoid Salmonella spp. is also unclear. Studies from Africa have shown
bacteraemia caused by non-typhoid Salmonella spp. to be common (Graham et al.;
2000, Berkley; et al. 2005) and often associated with malaria. Although the work of
Graham et al (2000) in Malawi has implicated non-typhoid Salmonella spp. in
radiological pneumonia cases, the role of these organisms in pneumonia is still
unclear, as blood-culture studies have focused on children with fever and fast
breathing and, therefore, may have identified children with bacteraemia only
(ODempsey et al., 1994).
The two causes of bacterial pneumonia that are vaccine-preventable are Hib and
pneumococcus (Mulholland; et al. 1997, Gessner; et al. 2005, Lagos; 1996, Baqui; et al. 2007, Cutts;
et al.; 2005, Klugman et al.; 2003, Madhi et al.; 2005). In both cases, the vaccines will preventmost pneumonia due to each pathogen, and microbiological methods will detect
only a few cases. Thus, the vaccine probe concept has emerged to describe
studies that are designed to determine the burden of pneumonia that can be
prevented by the vaccine, and is therefore attributable to the organism. These
studies have used the WHO definition of radiological pneumonia as the main
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outcome. For Hib, two randomized controlled trials (Mulholland; et al. 1997, Gessner; et
al., et al. 2005), one open trial (Lagos; et al. 1996) a casecontrol study with random
allocation of vaccine (Baqui; et al., et al. 2007) and several other casecontrol studies
have led to the conclusion that, in developing countries with a high burden of
pneumonia, 1530% of radiological pneumonia cases, and probably the same
proportion of pneumonia deaths, are due to Hib. For pneumococcus, three
randomized controlled trials in developing countries have shown that the nine-
valent pneumococcal conjugate vaccine can prevent 2035% of radiological
pneumonia cases and probably a similar proportion of pneumonia deaths (Cutts; et
al., et al. 2005, Klugman et tal.; 2003, Madhi; 2005). The newer pneumococcal vaccines
covering 1013 serotypes will likely extend this protection considerably. In
addition, one of the vaccines contains elements that may prevent non-typableH.
influenzae pneumonia as well. Thus, future pneumococcal vaccines may prevent
3050% of radiological and fatal pneumonia. WHO has recently established
modelled estimates of the number of pneumonia cases and deaths that are
attributable to these organisms on a country-by-country basis.
Pneumonia etiology studies that incorporate viral studies show that respiratory
syncytial virus is the leading viral cause, being identified in 1540% of pneumonia
or bronchiolitis cases admitted to hospital in children in developing countries,
followed by influenza A and B, parainfluenza, human metapneumovirus and
adenovirus (Weber et al.; 1999, Stensballe et al.; 2003). In the prospective microbiology-
based studies, viral causes of pneumonia are identified by rapid diagnostic tests
(such as indirect immunofluorescence, enzyme-linked immunosorbent assay,
polymerase chain reaction, viral culture on upper respiratory secretions such as
in nasopharyngeal aspirates or by viral serology in paired samples) (Weber;
Mulholland; Greenwood; 1999). It will be some time before any of these causes are
preventable by routine immunization.
Weber et al. (1998) made the most informative overview of respiratory syncytial
virus. Because this virus is fragile, it is difficult to detect and its importance is
probably underestimated. It was found in substantial frequency in all climatic and
geographical areas, with sharp peaks of activity over a period of 24 months, but
its seasonality varies considerably between regions. The peaks typically occur in
the cold season in temperate climates and in the rainy season in tropical climates.
Disease burden estimates from vaccine-probe studies are not yet available as for
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Hib and pneumococcus, but such data may become available from monoclonal
antibody trials, which show high efficacy against severe disease caused by
respiratory syncytial virus. Primary respiratory infection by this virus increases the
risk of secondary bacterial pneumonia and viral or bacterial coinfection is a
common finding in young children with pneumonia in developing countries
(approximately 2030% of episodes) (Forgie; et al. 2001). Furthermore, episodes of
wheezing due to reactive airways are more common after such episodes. Some
two-thirds of the episodes are seen in the first year of life, with 1.51.8 times
greater frequency in boys than in girls. This implies that any vaccination efforts
would need to be made early in life. The risk of pneumonia or bronchiolitis caused
by respiratory syncytial virus is highest among children aged less than 2 years with
the most severe disease occurring in infants aged 3 weeks to 3 months (Meissner;
2003, Weisman; 2003). A recent postmortem study of lung tissue samples from 98
Mexican children aged less than 2 years who died of pneumonia, which used
nested polymerase chain reactions, showed that 30% were positive for
respiratory syncytial virus: 62% of those with histopathological diagnosis of viral
pneumonia and 25% with diagnosis of bacterial pneumonia (Bustamante-Calvillo; et al.
2001). This study reaffirmed the role of respiratory syncytial virus as a very
significant and potentially deadly pathogen that causes childhood pneumonia,
both alone and through mixed infections with bacterial causes.
In recent years, the HIV epidemic has also contributed substantially to increases in
incidence and mortality from childhood pneumonia. In children with HIV,
bacterial infection remains a major cause of pneumonia mortality, but additional
pathogens (e.g. Pneumocystis jiroveci) are also found in HIV-infected
children(Klugman; Madhi; Feldman; 2007, Zar; Madhi; 2006), while M. tuberculosis remains
an important cause of pneumonia in children with HIV and uninfected children
(Meissner; 2003). Available vaccines have lower efficacy in children infected with
HIV, but still protect a significant proportion against disease (Zar; Madhi; 2006).
Antiretroviral programmes can reduce the incidence and severity of HIV-
associated pneumonia in children through the prevention of HIV infection, use of
co-trimoxazole prophylaxis and treatment with antiretrovirals (Zar; Madhi; 2006).
Other organisms, such asMycoplasma pneumoniae, Chlamydia spp., Pseudomonas
spp.,Escherichia coli, and measles, varicella, influenza, histoplasmosis and
toxoplasmosis, also cause pneumonia. Most of them are not preventable, but
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immunization against measles, influenza and possibly use of bacille CalmetteGurin (BCG) have probably contributed substantially to decreasing the
pneumonia burden. There are few data on the causes of neonatal pneumonia in
developing countries, but studies of neonatal sepsis suggest that these includeGram-negative enteric organisms, particularly Klebsiella spp, and Gram-positive
organisms, mainly pneumococcus, group b Streptococcus and S. aureus (WHO;
1999).
Pathophysiology
Bacteria commonly enter the respiratory tract but, due to multiple defense
mechanisms, do not normally cause pneumonia. When pneumonia does occur, it
usually is the result of an exceedingly virulent microbe, a large dose of bacteria,and/or impaired host defense exposure to overcrowded institutions such as
Streptococcus pneumoniae, Mycoplasmajails, shelters for homeless people,
militarypneumoniae, Chlamydia pneumonia training barracks, and childcare
centers Diabetic ketoacidosis S. pneumoniae, Staphylococcus aureus Chronic
obstructive pulmonary diseaseMoraxella catarrhalis Solid organ transplantation
(primarily from S. pneumoniae, Legionella pneumophila, immunosuppressant
drugs)M. catarrhalis Sickle cell disease (secondary to loss ofS. pneumoniae,
Haemophilus influenza splenic function) Cystic fibrosis S. aureus, Pseudomonas
aeruginosa Gastrointestinal surgeryEscherichia coli
When microorganisms evade upper respiratory defense mechanisms, the alveolar
macrophage is capable of removing most infectious agents without triggering a
significant inflammatory or immune response. However, if the microbe is virulent
or present in sufficiently high numbers, it can overwhelm macrophages and result
in a full-scale activation of systemic defense mechanisms. These mechanisms
include the release of multiple chemical mediators of inflammation, infiltration of
white blood cells, and activation of the immune response. Tight adherence of some
bacteria (e.g., Pseudomonas) to the tracheal lining and biofilm of an endotracheal
tube makes clearance of these microbes from the airways difficult and accounts, in
part, for their highly virulent nature.
In non-hospitalized people, bacteria reach the lung by one of four routes:
1. inhalation of microorganisms that have been releasUed into the air when an
infected individual coughs or sneezes
2. aspiration of bacteria from the upper airways
3. spread from contiguous infected sites
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4. hematogenous spread
When bacteria enter the lower respiratory tract, they adhere to the walls of bronchi
and bronchioles, multiply extracellularly, and trigger inflammation. Clinical risk
factors that favor colonization of the lower airways include antibiotic therapy thatalters the normal bacterial flora, diabetes, smoking, chronic bronchitis, and viral
infections.
With the onset of inflammation, alveolar air spaces fill with an exudative fluid (i.e.,
rich in protein). Inflammatory cells (first neutrophils during the acute phase, later
macrophages and lymphocytes during the chronic phase) subsequently invade the
walls of the alveoli.
Bacterial pneumonia may be associated with significant hypoxemia and
hypercapnia because thick, inflammatory exudate (or pus) collects in the alveolar
spaces and interferes with the diffusion of oxygen and carbon dioxide. Alveolarexudate tends to solidifya process known as consolidationand expectoration ofinfected phlegm becomes difficult. Legionella, Mycoplasma, and Chlamydia are
examples of atypical bacterial agents in that they produce patchy inflammatory
changes in the lungs (i.e., bronchopneumonia). The remaining typical bacterial
causes of pneumonia produce widespread inflammation throughout one or more
lobes of the lung (i.e., lobar pneumonia). Disease Summary Figure 13.1 illustrates
the distinguishing features of bronchopneumonia and lobar pneumonia. The term
double pneumonia is used to indicate the presence of infection and inflammation
within both lungs.
Disease Summary Table 13.3 Conditions That Interfere with PrimaryColonization of the pharynx and, possibly, the stomach with bacteria is the most
important factor in the pathophysiology of hospital-acquired pneumonia, followed
closely by aspiration of infected secretions into the lower airways. Pharyngeal
colonization is promoted by several exogenous factors: instrumentation of the
upper airways with contaminated nasogastric or endotracheal tubes, contamination
by dirty hands, and treatment with broadspectrum antibiotics that promote the
emergence of drug-resistant bacteria.
Although the role of the stomach in the pathophysiology of nosocomial pneumonia
remains controversial. However, research studies suggest that elevations in gastricpH resulting from the use of antacids, H2-receptor blockers, and enteral feeding
are associated with gastric microbial overgrowth and tracheobronchial
colonization.
Pneumococcal pneumonia remains the most common type of bacterial pneumonia
and its pathophysiology has been extensively studied. The initial step in the
development of this disease is the attachment of S. pneumoniae to cells of the
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nasopharynx and subsequent colonization. Colonization alone, however, does not
cause clinical manifestations of illness because perfectly healthy people can harbor
the microbe without evidence of infection.
Factors that permit pneumococci to spread beyond the nasopharynx include thevirulence of the strain, impaired host defense mechanisms, and viral infections of
the respiratory tract.Viruses can damage respiratory tract lining cells, enhance
bacterial adherence, and increase the production of mucus, which protects
pneumococci from phagocytosis. In the alveoli, pneumococci infect type II
alveolar cells and adhere to alveolar walls, causing an outpouring of fluid, red and
white blood cells, and fibrin from the circulation, which, in turn, results in
consolidation of the lung. Fluid in the lower airways creates a medium for further
multiplication of bacteria and aids in the spread of infection through pores of Kohn
into adjacent regions of the lung.
Diagnosis: Clinical Manifestations and Laboratory Tests
A diagnosis of bacterial pneumonia is based primarily on chest x-ray findings,
white blood cell count, and a sputum culture together with fever (often as high as
106F), recurrent chills, cough, shortness of breath (i.e., dyspnea), and abnormal
chest sounds.The clinical presentation of bacterial pneumonia varies from a mildly
ill, ambulatory patient to a critically ill patient with respiratory failure or septic
shock. The sudden onset of symptoms with rapid progression of the illness istypical of bacterial pneumonia. A thorough past medical history and history of
potential exposures are usually obtained.
Physical examination findings vary depending on the type of microorganism,
severity of pneumonia, age of the patient, coexisting host factors, and presence of
complications and may include the following investigations:
fever or hypothermia
rapid, shallow breathing
tachycardia or bradycardia
cyanosis decreased breath sounds
crackles (rales) with auscultation of the lungs
egophony on auscultation
pleural friction rub
dullness of the chest to percussion
altered mental status (especially confusion)
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Leukocytosis (15,000 white blood cells/mm3) with a shift to the left and apredominance of neutrophils in the circulation may be observed with any bacterial
infection. However, its absence, particularly in patients who are elderly or
debilitated, should not cause the clinician to discount the possibility of a bacterialinfection. Leukopenia is an ominous sign of impending sepsis and portends a poor
outcome. An assessment of the arterial blood gases is essential to determine if
hospital admission or oxygen supplementation is indicated and may reveal
hypoxemia and respiratory acidosis. A pulse oximetric finding that is 90%
indicates significant hypoxemia.
Hyponatremia and microhematuria may be associated withLegionella pneumonia.
Urinary antigen testing forLegionella serogroup 1 microbes is accurate. A
Legionella serum antibody titer of 1:128 or more is suggestive ofLegionella
pneumonia. The presence ofMycoplasma and Chlamydia immunoglobulin Mantibodies contribute to the diagnosis.
Chest radiographs reveal white shadows in the involved area indicative of an
alveolar.
Disease Summary Table 13.6 Preferred Pharmacotherapy forMicroorganism Common Clinical Manifestations Gram Stain ResultStaphylococcus aureus Fever, chills, chest pain, productive
cough, yellow sputum
Streptococcus pneumoniae Fever, chills, chest pain, productive
cough, malaise, fine crackles, rust-
colored sputum
Haemophilus influenzae green sputum Upper respiratory symptoms, fever,
vomiting, irritability, productive cough,
spnea
Klebsiella pneumoniae Productive cough, sputum is thick and
dark red
Pseudomonas aeruginosa Fever, chills, copious green and foul-
smelling sputum
Legionella species Fever, vomiting, diarrhea, myalgia,abdominal pain, malaise, weakness,
lethargy, dry cough, fatigue, low-grade
fever
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ManagementThe primary goals of treatment are to eradicate the infection, reduce morbidity, and
prevent complications. The pneumonia severity of illness scoring system (PSISS)
evaluates 19 different characteristics of the patient that are easily obtained. ThePSISS is used to make a decision whether patients can be safely treated in an
outpatient setting.
Patients in risk class I (older than 50 years but no coexisting illness or vital sign
abnormality) and risk class II (70 total points) can be treated at home with planned
outpatient follow-up evaluations. Patients in risk class III (7190 total points)
should be observed in the emergency room before their disposition is decided.
Patients in risk class IV (91130 total points) and V (130 total points) are seriously
ill and usually require hospital admission.
Since many patients are hypoxemic, the first step in the management of bacterialpneumonia is establishing adequate ventilation and oxygenation. For patients with
mild dyspnea, only supplemental low-flow oxygen administered with a nasal
cannula may be required. Patients with underlying chronic lung disease who need
high oxygen concentrations may require endotracheal intubation. Other important
measures include the following:
adequate hydration to loosen secretions and help bring up phlegm
correction of serum electrolyte abnormalities
control of fever with antipyretic agents
bedrest
good pulmonary hygiene (e.g., deep breathing and coughing exercises, suction ofsecretions, chest physical therapy)
Early mobilization of patients with encouragement to sit, stand, and walk when
tolerated also speeds recovery.
The mainstay of pharmacotherapy for bacterial pneumonia is antibiotic treatment.
Antibiotic therapy should be initiated promptly after the diagnosis is established
and appropriate specimens are obtained, especially in patients who require
hospitalization. Delays in obtaining diagnostic specimens or the results of testing
should not preclude the early administration of antibiotics to acutely ill patients.
The choice of pharmacotherapeutic agent(s) is based on the severity of thepatients illness, host factors (e.g., coexisting illness and age), and the presumed or
identified causative agent. Outpatients are given oral agents and, for the most part,
parenteral medications are given to hospitalized patients.
Complications and Prognosis
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Potential serious complications of bacterial pneumonia are multiple and include the
following:
local destruction of lung tissue with subsequent scarring and significant loss of
gas exchange. bronchiectasis.
empyema (i.e., accumulation of pus in the pleural space that often requiressurgery and aspiration).
respiratory failure. dependence on mechanical ventilation.
septic shock.
Prognosis generally is good in the otherwise healthy patient with uncomplicated
pneumonia.
With appropriate treatment, most patients improve markedly within 2 weeks.Several factors, alone or in combination, increase morbidity and mortality and
include the following:
advanced age.
aggressive microbes (e.g., Klebsiella,Legionella).
coexisting illness. development of respiratory failure.
CONCEPTUAL FRAME WORK
Utilizing Neumanss system model, (Neuman & Fawcett) it emphasis on line ofdefense inherent in man. They stresses the flexibility of these line of defense such
that the human defense depends on the strength of these lines. It further models
Nursing intervention to focus threatening and maintaining system stability. The
interventions to be carried out are base on: Primary, Secondary and Tertiary
preventions.
Also in cooperating Nightingales Everonmental theory, there is need for keeping
clients warm, maintaining noise-free environment, and attainding to clients diet in
terms of intake, timeliness of food and its effect on the client/person should be
noted.Utilizing these theories in the management of bronchopneumonia, prognosis is
usually favorable.
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CHAPTER THREE
RESEARCH METHODOLOGY
This chapter deals with the method to be employed for this study.
Research Design
This is a comparative historic research design conducted to find out the incidence
and management outcome of bronchopneumonia among children 1-5 yearsadmitted into children medical ward of University of Port Harcourt Teaching
Hospital.
Research Setting
The University of Port Harcourt Teaching Hospital (UPTH) is one of the 3rd
generation Teaching Hospitals established by law in 1985 via Decree No. 10 of
1985, though it commenced operation in 1980. The mandates (statutory functions)
of the hospital are: To train and develop health manpower for the country especially in the
catchment population of the Niger Delta region.
To provide and render specialized (tertiary) health services to the Nigerianpopulace.
To engage in health and medical research for the expansion of the frontiersof knowledge and practice of medicine.
The University of Port-Harcourt Teaching has operated from two Temporary Sites
since inception in 1980. The Permanent Site of the Hospital has been underdevelopment since 1982, i.e. over twenty-five years. This circumstance had placed
some limitations on the development of infrastructure and services in the Hospital.The Hospital has:
Evolved from a 60-bed hospital to a 500+ bed hospital
Transited from the last Temporary Site to an ultra modern Permanent Site
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in October, 2006.
Managed through a three-tier managerial structure comprising - the
Board of Management, Hospital Management Committee (HMC) and theDepartments.
Delivers services at primary, secondary and tertiary levels.
Services delivered through a good crop of well trained and experienced staff
comprising:
About 100 medical Specialists/Educators (Consultants)
About 300 trainee specialist (resident) doctors.
About 100 trainee house officers
Over 300 well trained and experienced nursesOver 300 other categories of paramedical staff
Trained over 1500 medical students as doctors, over 1000 house officers and
over 50 medical specialists (consultants), all cadres of Nursing, Pharmacy,
Laboratory, etc, staff have also benefited from continuous education and
trainings.
Treats over 150,000 outpatients per year, 10,000 in-patients per year, and
perform over 3000 surgical operations per year. The average all year round
bed occupancy rate is over 70 percent.
Well over 1000 high quality research activities have been carried out in
UPTH with the results published in major National and International
Medical and Scientific journals.
Primary Health Care
Primary Health Centre, Aluu, Ikwerre Local Government Area, Rivers
General Outpatient clinic, UPTH, Port Harcourt
Accident and Emergency Centre (Medical/Trauma)
Children's Emergency Room (Paediatrics Emergencies)
Immunization Clinic
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Secondary/Tertiary Health Care
Internal Medicine
Endocrinology
Cardiology
Gastroenterology
Neurology
Respiratory Medicine
Nephrology
Dermatology
Venerology/STDs ClinicsHIV/AIDS Clinic
Surgery
General Surgery
Urology
Burns and Plastics
Cardiothoracic
Orthopaedics/Trauma
Paediatrics SurgeryPaediatrics- the Unit that houses the ward (children medical wards) at
which the research is conducted.
Neonatology
Nephrology
Neurology
Gastroenterology
Social Paediatrics/Nutrition
RespiratorySchool Health Programme
Obstetrics and Gynaecology
Oncology
Fertility
Prevention of Mother to Child Transmission on HIV/AIDS
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Target population
The targets populations are children within the age range of one-five years
(1-5 years) admitted into the medical ward of University of Port Harcourt
Teaching Hospital and are managed for bronchopneumonia.
Sample and Sampling Techniques
Criteria for inclusion for the study were Children (1-5 yrs) whom were diagnosed
of bronchopneumonia and managed in the medical ward of University of Port
Harcourt Teaching hospital and whom there medical records were accessible
within the time frame of study. A written letter was directed to the head of
General Obstetrics/Gynaecology
Ophthalmology
Ear, Nose and Throat (ENT) SurgeryDentistry
Physiotherapy
Radiology
Morbid Anatomy
Haemetology and Blood Transfusion/immunology
Chemical Pathology
Medical Microbiology/Parasitology
Anaesthesiology
Intensive Care Medicine
Occupational Therapy
Neuropsychiatry
General Medical Practice (Family Medicine)
Most of the sub-specialties within these major clinical specialties are under-
developed and unaccredited for sub-specialty training.
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medical records stating the purpose of reviewing patients medical records and
permission were granted. My subjects were gotten through reviewing of
admission records from 2009-2011 of children Medical wards of whom werediagnosed bronchopneumonia.
This is to ensure that at least 97% of children diagnosed and managed of
bronchopneumonia are studied.
Instrument of Data Collection
After determining what information that was needed, data for the research were
collected from the admission and discharge ofpatients medical record ofUniversity of Port Harcourt Teaching Hospital, Rivers state.
This informations of interest were designed to evaluate the incidence rate,management outcome and knowledge base of parents to children diagnosed ofbronchopneumonia.
Validity of Instrument
The instrument for date collections are valid and reliable due to the fact that they
are gotten from the patients medical record chart and will always give the sameinformation in the same patients in further study.
In addition, my supervisors suggestions were also incorporated accordingly.
Reliability of the Instrument
The reliability of the instrument is based on the fact that the date was gotten from
the primary source and as such, will always give same information in futurereview.
Method of Data Collection
Data collected from the medical records of University of Port Harcourt Teaching
Hospital were analysed and represented in a tabular form with arithemetic
percentage worked out.
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Data Preparation and Analysis
The data was analyzed in terms of frequency distribution, percentage and cross
tabs utilizing the SPSS computer program. Cross tabulations were used to describethe relationship between the variables of incidence of bronchopneumonia and
management. Pearsons Product Moment Correlation Coefficient was employed totest the hypotheses. The statistical analysis was determined at 0.05 significant evel.
Ethical Considerations
The researcher applied to the ethical committee in the University of Port-Harcourt
for permission to carry out the research and it was granted.
The respondents were informed of the study and their consent duly obtained.
The benefits to be derived from the study and the issue of confidentiality were
stressed.
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