project paediatric

7/31/2019 Project Paediatric

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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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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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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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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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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.

project paediatric

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