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 having bronchopneumonia (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 patients were 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 host tissues 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 usually results 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 become obstructed, 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 to overcome 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 focal sites, 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 Clinical Presentation). 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 airways leads 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 interstitium is 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 mixed pattern 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 the incidence (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 prognosis of the disease. Statement of the problem Despite the health education given to mothers in their Ante-Natal and Post-Natal routine 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 Pneumonia especially bronchopneumonia.
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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 bronchopneumonia within 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 20092011 in children medical ward? 2. What is the management outcome of bronchopneumonia of children (1-5 years) in UPTH? 3. What is the educational status of Parents whose children are diagnosed of bronchopneumonia? 4. What is the economic status of parents whose children are diagnosed of bronchopneumonia? Hypothesis There is a significant relationship between Economic and Educational status of parents 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. Available
from: 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
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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 the estimated 156 million global episodes. More than half of the worlds annual new pneumonia cases are concentrated in just five countries where 44% of the worlds children 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 28 community-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 for calculating 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 < 2) Low birth weight ( 2500 g) Non-exclusive breastfeeding (during the first 4 months of life) Lack of measles immunization (within the first 12 months of life) Indoor air pollution Crowding
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Likely risk factors Parental smoking Zinc deficiency Mothers experience as a caregiver Concomitant diseases (e.g. diarrhoea, heart disease, asthma) Possible risk factors Mothers 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) and Haemophilus 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 blood cultures 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 and H. 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 of pneumonia 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 is directed (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 significant fraction 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-typable H. 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 of H. 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, found S. 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 nontyphoid 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 prevent most 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 ninevalent 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-typable H. 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 microbiologybased 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 HIVassociated pneumonia in children through the prevention of HIV infection, use of co-trimoxazole prophylaxis and treatment with antiretrovirals (Zar; Madhi; 2006). Other organisms, such as Mycoplasma 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 Calmette Gurin (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 include Gram-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, Mycoplasma jails, shelters for homeless people, military pneumoniae, Chlamydia pneumonia training barracks, and childcare centers Diabetic ketoacidosis S. pneumoniae, Staphylococcus aureus Chronic obstructive pulmonary disease Moraxella catarrhalis Solid organ transplantation (primarily from S. pneumoniae, Legionella pneumophila, immunosuppressant drugs) M. catarrhalis Sickle cell disease (secondary to loss of S. pneumoniae, Haemophilus influenza splenic function) Cystic fibrosis S. aureus, Pseudomonas aeruginosa Gastrointestinal surgery Escherichia 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 that alters 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. Alveolar exudate tends to solidifya process known as consolidationand expectoration of infected 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 Primary Colonization 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 gastric pH 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 the virulence 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 is typical 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 a predominance 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 bacterial infection. 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 with Legionella pneumonia. Urinary antigen testing for Legionella serogroup 1 microbes is accurate. A Legionella serum antibody titer of 1:128 or more is suggestive of Legionella pneumonia. The presence of Mycoplasma and Chlamydia immunoglobulin M antibodies contribute to the diagnosis. Chest radiographs reveal white shadows in the involved area indicative of an alveolar. Disease Summary Table 13.6 Preferred Pharmacotherapy for Microorganism Common Clinical Manifestations Gram Stain Result Staphylococcus aureus Fever, chills, chest pain, productive cough, yellow sputum Streptococcus pneumoniae Fever, chills, chest pain, productive cough, malaise, fine crackles, rustcolored 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 foulsmelling sputum Legionella species Fever, vomiting, diarrhea, myalgia, abdominal pain, malaise, weakness, lethargy, dry cough, fatigue, low-grade fever
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Management The 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. The PSISS 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 bacterial pneumonia 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 of secretions, 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 the patients 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 requires surgery 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 of defense 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 years admitted 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 Nigerian populace. To engage in health and medical research for the expansion of the frontiers of 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 under development 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 the Departments. 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 nurses Over 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 Clinics HIV/AIDS Clinic Surgery General Surgery Urology Burns and Plastics Cardiothoracic Orthopaedics/Trauma Paediatrics Surgery Paediatrics- the Unit that houses the ward (children medical wards) at which the research is conducted. Neonatology Nephrology Neurology Gastroenterology Social Paediatrics/Nutrition Respiratory School Health Programme Obstetrics and Gynaecology Oncology Fertility Prevention of Mother to Child Transmission on HIV/AIDS
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General Obstetrics/Gynaecology Ophthalmology Ear, Nose and Throat (ENT) Surgery Dentistry 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 underdeveloped and unaccredited for sub-specialty training.
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
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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 were diagnosed 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 of patients medical record of University 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 of bronchopneumonia. 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 same information 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 future review.
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 describe the relationship between the variables of incidence of bronchopneumonia and management. Pearsons Product Moment Correlation Coefficient was employed to test 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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INCIDENCE AND MANAGEMENT OUTCOME OF BRONCHOPNEUMONIA IN CHILDREN (1-5 yrs.) IN UPTH

Data Preparation and Analysis

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