i

CLINICAL PREDICTORS OF HYPOXAEMIA IN UNDER-

FIVE CHILDREN WITH PNEUMONIA AT THE UNIVERSITY

OF ILORIN TEACHING HOSPITAL

A DISSERTATION SUBMITTED TO THE NATIONAL

POSTGRADUATE MEDICAL COLLEGE OF NIGERIA IN PART

FULFILMENT OF THE REQUIREMENTS FOR THE FELLOWSHIP

OF THE COLLEGE IN PAEDIATRICS

DR RASHEEDAT MOBOLAJI IBRAHEEM

MBBS (IBADAN) 2002

MAY, 2013

ii

DECLARATION

I, DR. RASHEEDAT MOBOLAJI IBRAHEEM, hereby declare that this dissertation is

original unless otherwise acknowledged. The dissertation has not been presented to any

college for fellowship examination.

_______________________________

DR. IBRAHEEM R.M.

iii

CERTIFICATION

We hereby certify that Dr. Rasheedat Mobolaji Ibraheem of the Department of Paediatrics

and Child Health, University of Ilorin Teaching Hospital, Ilorin prepared this dissertation

under our close supervision.

1. SIGNATURE ___________________________________

NAME OF SUPERVISOR Prof ‘Wahab B.R. Johnson

2. SIGNATURE _________________________________

NAME OF SUPERVISOR Dr. Aishat A. Gobir

iv

DEDICATION

This dissertation is dedicated to God Almighty, the fountain of knowledge and health who enabled

me to do this work, and to all children who ever had pneumonia.

v

ACKNOWLEDGEMENT

With utmost humility and gratitude, I wholeheartedly acknowledge the Almighty God in the

pursuit of my career, and for giving me the grace to do this work. I thank my parents, most

especially my late father, who put my feet in this noble profession, and for their ever ready

support and help. I acknowledge my able supervisors, Professor ‘W.B.R. Johnson and Dr.

A.A Gobir, for always finding time for me from their busy schedule. I am immensely grateful

to Prof. Johnson who has been not only a supervisor but also a mentor throughout the

residency program. My immense gratitude goes to Emeritus Professor Adeoye Adeniyi, who

has availed me of his knowledge and experience despite retirement, and to Professors A.

Ojuawo, O.A. Mokuolu and O.T. Adedoyin. My profound gratitude also goes to my able

teachers, Drs S.K. Ernest, O.A. Adegboye, O.A. Adesiyun, J.K. Afolabi and M.A.N.

Adeboye, who out of their busy schedule found time to give advice, criticism, encouragement

and direction in the art of research and scientific writing.

I thank Drs. A. Fadeyi, H. Ekundayo and Mrs. R. Abubakar, all of the Department of

Microbiology, for their help during the laboratory analysis. The same goes for Dr. K. Jimoh

of the Radiology Department and Dr. R.O. Oladosu of the Haematology Department. I am

also greatly indebted to Dr. A. Oyeyemi of the Statistics Department, University of Ilorin for

deploying his expertise in assisting with the statistical analysis and for always willing to

explain and demystify the copious statistical analysis required.

I am deeply grateful to my senior colleagues in the department, Drs. A. Saka and M.B.

Abdulkadir for their encouragement and support. I am grateful for the support and assistance

rendered by all the members of the department; nurses, house officers especially Drs

Oyeyemi, Oyinloye and Agaja, and my co-residents.

I acknowledge the encouragement, kindness and support of my mother-in-law, Mrs B.A.

Ibraheem. To my aunt, Mrs Iyabo Ogunbiyi who looked after my children whenever I needed

Commented [MA1]: hope no change of name issues

vi

to be away for long hours (at one stage or the other of the residency training), I am indeed

grateful. My siblings and brothers-in-law are all appreciated for their understanding and

support during the ‘trying period’ of my residency training.

Finally, I am immensely grateful to my darling husband, Dr Gbadebo Ibraheem, for his

unwavering love, support and help at all times, and my children, Jibril, Haneefah and Aishat,

who endured many long days and nights without my company in my pursuit of academic and

professional goals.

To all my benefactors in accomplishing this research project, God bless you all.

vii

TABLE OF CONTENTS

Title page i

Declaration ii

Certification iii

Dedication iv

Acknowledgement v

Table of contents vii

List of Tables ix

List of Figures xi

List of abbreviations xii

Glossary of terms xiv

Summary xv

Introduction 1

Literature review 4

Justification 42

Aims and objectives 44

Materials and Method 45

Results 54

Discussion 77

Conclusions 88

Recommendations 89

Limitations of the study 90

References 91

Appendices

I. Information sheet 102

viii

TABLE OF CONTENTS continued Page

II. Informed consent form 104

III. Study proforma 105

IV. Social class classification 111

V. British Thoracic Society (BTS) Guidelines on childhood CAP 112

VI. UITH ethical committee approval 113

VII. National Postgraduate Medical College of Nigeria (NPMCN) approval 114

ix

LIST OF TABLES PAGE

Table I: Limitations of pulse oximeter 17

Table II: Common agents causing community-acquired pneumonia based on age 29

Table III: Severity assessment of pneumonia 38

Table IV: Options of antibiotics in relation to age and clinical presentation of CAP 39

Table V: Age and gender distribution of the children with pneumonia 54

Table VI: Some risk factors of pneumonia in the study population 55

Table VII: The physical examination findings in children with pneumonia 57

Table VIII: Anthropometric measurements in children with pneumonia 58

Table IX: Bacterial agents of pneumonia in the subjects 59

Table X: Hypoxaemia and SpO2 levels in children with pneumonia 60

Table XI: Hypoxaemia based on the severity and type of pneumonia 61

Table XII: Pneumonia symptoms as predictors of hypoxaemia in the subjects 62

Table XIIIA: Clinical parameters as predictors of hypoxaemia in the children

with pneumonia-I 63

Table XIIIB: Clinical parameters as predictors of hypoxaemia in the children

with pneumonia-II 64

Table XIV: Linear regression model of the clinical features and the presence of

hypoxaemia in children with pneumonia 65

Table XVA: Hypoxaemia and risk factors of pneumonia in the study

Population-Group 1 66

Table XVB: Hypoxaemia and risk factors of pneumonia in the study

Population-Group 2 67

Table XVI: Correlation of the risk factors of pneumonia with the presence of

hypoxaemia 68

Table XVII: Pneumonia-associated complications and hypoxaemia in the subjects 70

Table XVIII: Hypoxaemia and treatment outcome in the children with pneumonia 71

x

LIST OF TABLES continued Page

Table XIX: The pulse oximeter reading and outcome in children with pneumonia 72

Table XX: The duration of hospitalization and hypoxaemia in children with pneumonia 74

Table XXI: The duration on oxygen therapy and hypoxaemia in the study population 76

xi

LIST OF FIGURES PAGE

Figure 1: Diagram of the respiratory tract 5

Figure 2: Diffusion of gases across the alveolar–capillary membrane 7

Figure 3: Pathophysiology of respiratory signs in pneumonia 9

Figure 4: Common pulsatile signals on a pulse oximeter 15

Figure 5 Symptoms of pneumonia in the study population 56

Figure 6: Complications of pneumonia in the study population 69

xii

LIST OF ABBREVIATIONS

1. ABG - Arterial blood gases

2. AIDS - Acquired immumodeficiency syndrome

3. ALRI - Acute lower respiratory infections

4. ARI - Acute respiratory infections

5. AURI - Acute upper respiratory infections

6. BBS - Bronchial breath sounds

7. BTS - British Thoracic Society

8. CAP - Community acquired pneumonia

9. CIE - Counterimmunoelectrophoresis

10. CO2 - Carbon dioxide

11. 0C -Degree Centigrade

12. DAMA -Discharge against medical advice

13. EPU -Emergency Paediatric Unit

14. g/L -Grams per Litre

15. Hb - Haemoglobin

16. Hib -Haemophilus influenzae type b

17. HIV - Human immunodeficiency virus

18. LAT - Latex agglutination test

19. µ -Micro

20. mg/dl -Milligram per deciliter

21. mls -Millilitres

22. mmHg -Millimeters of Mercury

23. mmol/L -Millimole per Litre

24. nm -Nanometer

xiii

LIST OF ABBREVIATIONS continued

25. O2 - Oxygen

26. ODC - Oxygen-haemoglobin dissociation curve

27. PaO2 - Partial pressure of oxygen in arterial blood

28. PaCO2 - Partial pressure of carbon dioxide in arterial blood

29. PCR - Polymerase chain reaction

30. PiO2 - Inspired partial pressure of oxygen

31. RBC -Red blood cell

32. SpO2 - Haemoglobin oxygen saturation

33. 2,3-DPG - 2,3 diphosphoglycerate

34. UITH -University of Ilorin Teaching Hospital

35. WBC -White blood cell

36. WHO - World Health Organization

xiv

GLOSSARY OF TERMS

Wheeze: a high pitched musical whistling noise, often heard at expiration with

corresponding prolongation and increased effort of expiration, emanating from the

intrathoracic airway.

Nasal flaring: widening of the alae nasi as the child breathes in.

Rhonchi: an audible wheeze using a stethoscope.

Crepitations: are discontinuous, interrupted explosive sounds audible with a

stethoscope, which may be coarse (loud, low pitched) or fine (high-pitched).

Central cyanosis: bluish discoloration of the tongue and buccal mucosa due to the

presence of > 5 g/dl of deoxygenated (reduced) haemoglobin.

Chest wall indrawing: inward movement of the lower chest wall on breathing in.

Sensitivity: is the probability that individuals with the disease would be correctly

identified as having the disease by the diagnostic test.

Sensitivity = _______True Positive________

True Positive + False Negative

Specificity: is the probability that individuals without the disease would be correctly

identified as not having the disease by the diagnostic test.

Specificity = ______True Negative_______

True Negative + False Positive

Positive predictive value (PPV): is the probability that individuals who test positive

for the disease actually have the disease.

PPV = _______True Positive_____

True Positive + False Positive

Negative predictive value (NPV): is the probability that individuals who test

negative for the disease are really disease free.

NPV= _______True Negative_______

True Negative +False Negative

xv

SUMMARY

Hypoxaemia constitutes a possible complication of severe respiratory illness which is often

under-reported in developing countries. In view of this, the current study was carried out to

determine the prevalence and clinical predictors of hypoxaemia in hospitalized under-five

children with pneumonia in Ilorin. An association between the risk factors of pneumonia and

hypoxaemia, as well as the relationship between various levels of hypoxaemia and the

management outcome of pneumonia were also explored.

This is a descriptive cross-sectional study of 200 children aged between two months and five

years with pneumonia recruited consecutively as subjects. Socio-demographic,

anthropometric, clinical and laboratory data were obtained, while the admission diagnosis

was based on clinical features. The pulse oximetry measurement was recorded after a stable

reading for at least one minute while the child was breathing room air. Hypoxaemia was

defined as an arterial oxygen saturation of less than 90% as recorded by pulse oximetry

Blood samples were collected for determining the packed cell volume, total and differential

white blood cell (WBC) count and blood cultures. Also, chest radiographs were obtained in

all subjects. Data was analyzed using the IBM®SPSS 20.0 (2011) software package.

There were 119 males and 81 females (M:F=1.5:1). Severe pneumonia was present in 188

(94.0%) children while 12(6.0%) children had moderate pneumonia. Bronchopneumonia was

identified in 168(84.0%) of the children while lobar pneumonia was diagnosed in 32(16.0%)

children. The prevalence of hypoxaemia in the children with pneumonia was 41.5%.

Using a linear regression analysis, the clinical features that were significantly associated with

hypoxaemia were restlessness, lower chest wall indrawing, bronchial breath sounds and

tender hepatomegaly (p <0.05). Restlessness had a sensitivity of 22.9%, specificity of 91.5%,

positive predictive value (PPV) of 65.5% and a negative predictive value (NPV) of 62.6%,

while chest wall indrawing had a sensitivity of 86.7%, specificity of 53.3%, PPV of 56.7%

xvi

and NPV of 84.9% for detecting hypoxaemia. Bronchial breath sound had a poor sensitivity

(16.9%), a high specificity (95.7%), PPV of 73.7% and a NPV of 61.9%, whereas tender

hepatomegaly had a sensitivity of 48.2%, specificity of 82.9%, PPV of 66.7% and a NPV of

69.3%.

There was a negative correlation between the social class of the child and the presence of

hypoxaemia (r= -0.191, p=0.007). Also, each of maternal age (years), maternal literacy level,

birth order of the child and lack of immunization had a negative correlation with the presence

of hypoxaemia (r= -0.151, -0.162, -0.154, -0.148; p=0.032, 0.022, 0.030 and 0.036

respectively).

Seventeen of the children with pneumonia died, giving a corresponding case fatality of 8.5%.

The mean(SD) SpO2 level of 78.3(10.9) percent recorded among the fatal cases was

significantly lower compared to the corresponding value of 91.5(7.8) percent recorded in the

survivors (p=0.001). The mean(SD) duration of hospitalization in hypoxaemic children of

6.9(6.4) days was significantly longer compared to the corresponding value of 4.9(2.7) days

recorded in those without hypoxaemia (p=0.002). Also, the mean duration of hospitalization

increased significantly as the SpO2 levels reduced (p=0.002).

It is concluded that there is a high local burden of pneumonia-associated hypoxaemia and that

hypoxaemic-related pneumonia is frequently associated with a fatal outcome. It is

recommended that pulse oximeters be made available in facilities where pneumonia is

managed. There is also a need to emphasize the potential value of clinical parameters like

restlessness, lower chest wall indrawing, bronchial breath sounds and tender hepatomegaly

for detecting pneumonia-related hypoxemia in poorly equipped health facilities.

1

INTRODUCTION

Globally, pneumonia remains a leading cause of death among under-five children, with

pneumonia accounting for over 90% of ALRI-related deaths.1 In Nigeria, pneumonia-related

deaths account for 20-25% of childhood mortality; the estimated median incidence of

pneumonia is 34 per 100 child years, with approximately 6.1 million new cases annually.1, 2

Previous studies from Ilorin in the North-Central regions of Nigeria have shown a mean

incidence of pneumonia of 1.3 episodes per child-year in under-five children and a case

fatality rate of 10% respectively.3, 4 These pneumonia-related deaths may be ascribed to one

or more of dissemination of the causative pathogens, or ventilation-perfusion mismatch with

resultant hypoxaemia and subsequent respiratory failure.5 Hence, the advent of hypoxaemia

constitutes a grave manifestation of severe respiratory illness.

Traditionally, the levels of arterial blood gases are used for monitoring hypoxaemia in

patients with pneumonia, but more recently the use of pulse oximeters has been gaining

ground in many health facilities. As a non-invasive, simple and reproducible method of

measuring the arterial haemoglobin oxygen saturation (SpO2), pulse oximetry remains a

reliable bedside tool for monitoring the level of hypoxaemia in clinical practice.6 In a 2009

systematic review, the median prevalence of hypoxaemia in ill children using WHO-defined

pneumonia was 13.0% in developing countries, varying with a prevalence rate of 3.0-10.0%

in Africa and 9.0-39.0% in Asia.7 Despite the morbidity burden of pneumonia in the African

sub-region, the limited data on ALRI-related hypoxaemia have emanated from a few

countries like Kenya, the Gambia, and Zambia.8-12 To the best of the knowledge of this

researcher, there is a clear paucity of accessible data on pneumonia-related hypoxaemia in

Nigerian children.

Various clinical symptoms and signs have been studied for their ability to predict hypoxemia

in children with pneumonia.13-16 The major symptoms and physical signs associated with

2

hypoxaemia include central cyanosis, altered mental state, tachypnoea, chest wall retractions

and the use of accessory muscles of respiration. Although the reported sensitivity and

specificity of these signs varied widely in some earlier studies, the presence of respiratory

rates above age specific cut-off values and lower chest indrawing were reported as highly

specific and sensitive. Hence, these clinical parameters were considered useful for identifying

hypoxaemia.16,17 On the other hand, physical signs such as central cyanosis, grunting and

head nodding had earlier been identified as poorly sensitive but nevertheless specific clinical

predictors of hypoxaemia.9,13-15 The current study was therefore aimed at determining the

ability of clinical symptoms and signs to predict hypoxaemia in children with pneumonia in

Ilorin, North Central Nigeria.

Socio-demographic factors such as the age, sex, parental income, and level of parental

education, had earlier been identified as risk factors of pneumonia-related morbidity and

mortality.18-20 Also domestic crowding, maternal age/child care experience, exposure to

indoor air pollutants especially firewood burning, and parental smoking had each been

recognized as important domestic/household risk factors.21,22 Other factors identified by

earlier studies included attendance at day care facilities, breastfeeding practices,

malnutrition, co-morbidities like diarrhoea, HIV/AIDS, micronutrient deficiency (especially

vitamin A and zinc), and inter-current infections such as measles and pertussis.23-27 Despite

the current body of knowledge linking these risk factors with the frequency of pneumonia and

a fatal outcome, there is still a dearth of published data assessing the association between

these risk factors of pneumonia and the occurrence of hypoxaemia.

Given the association between hypoxaemia and a fatal disease outcome, the dire need for an

early detection of hypoxaemia and prompt oxygen therapy in children with ALRI is hardly

contestable. Hence, with a view to preventing an adverse outcome, the identification of

certain clinical signs which are predictive of hypoxaemia may be a crucial part in the clinical

3

management of under-five children with pneumonia. Undoubtedly, the identification of

predictive clinical clues of hypoxaemia by the current study will guide the formulation of

rational guidelines for initiating oxygen therapy in children with pneumonia and improve the

disease outcome of children with pneumonia. Ultimately this will reduce the corresponding

disease-related mortality. It is envisaged that this will be a significant step towards

formulating health policies for accomplishing the fourth Millennium Development Goal

(MDG), namely a reduction by two-thirds of the national under-five mortality rate in Nigeria

by 2015.

4

LITERATURE REVIEW

Anatomy of the respiratory tract

The respiratory tract is made up of the organs involved in breathing, transport and exchange

of respiratory gases. It can be divided into a conducting portion (naso-oropharynx, larynx,

trachea, bronchi, bronchioles) which carries the gases during inspiration and expiration and a

respiratory portion (alveoli in the lungs) which provides for gas exchange.28 A thin epithelial

basement membrane forms the outer layer of the alveolar wall, and a dense network of

capillaries surrounds each alveolus. The basement membranes of the alveolus and the

capillary network are in close proximity, creating an air–blood interface.

The part of the respiratory system which contains gas that is not available for gaseous

exchange with pulmonary capillary blood constitutes the dead space.28 This space comprises

the anatomic dead space (respiratory system volume exclusive of alveoli), and the

physiologic dead space (volume of gas not equilibrating with blood). In healthy individuals

the two dead spaces are identical. However in disease states such as atelectasis and

pneumonia, there may be no exchange between the gas in some of the alveoli and the blood,

either as a result of compensatory under-perfusion or overventilation of some of the alveoli.

The upper respiratory tract consists of the airways from the nostrils to the vocal cords in the

larynx (including the paranasal sinuses and the middle ear) while the lower respiratory tract

covers the continuation of the airways from the trachea and bronchi to the bronchioles and

the alveoli (Figure 1).29 Thus, infections involving anatomic areas above the defined

boundary are regarded as upper respiratory infections, while those below are referred to as

lower respiratory infections. With the larynx, particularly the vocal cords, chosen as the

demarcation between the upper and lower tracts, epiglottitis is subsumed as a diagnostic

entity along with nasopharyngitis, sinusitis, pharyngitis (pharyngotonsillitis) and otitis media

as acute upper respiratory infections (AURI).30, 31 Acute lower respiratory infections (ALRI)

5

comprise tracheo-bronchitis, bronchiolitis and pneumonia. The latter ALRI syndrome

(pneumonia) constitutes a major cause of hypoxaemia and indeed the commonest cause of

ALRI-associated death.

Figure 1: Anatomy of the respiratory tract (Image source-http://en.wikipedia.org/wiki/Lower respiratory tract&usg.com)

Pulmonary physiology

The goals of respiration are to provide oxygen to the tissues and to remove carbon dioxide.

These goals are achieved through four major functions:

1. Pulmonary ventilation which involves the inflow and outflow of air between the

atmosphere and the lung alveoli.

2. Diffusion of oxygen and carbon dioxide between the alveoli and the blood – gas

exchange.

3. Transport of oxygen and carbon dioxide in the blood and body fluids to, and from the

body's tissue cells.

4. Regulation of ventilation and other aspects of respiration.

6

Mechanics of pulmonary ventilation: Pulmonary ventilation is achieved through sequential

expansion and emptying of the lungs in two ways. The mechanical processes consist of either

downward and upward movement of the diaphragm (to lengthen or shorten the height of the

chest cavity) or the elevation and depression of the ribs (to increase or decrease the antero-

posterior diameter of the chest cavity).28 Normal quiet breathing is accomplished almost

entirely by the first process, while the second occurs during heavy breathing and involves the

use of the accessory muscles of inspiration and expiration, especially the intercostal

muscles.28

Compliance is the term used to describe the elasticity or distensibility of tissues and organs of

the respiratory pump such as the lungs and chest wall.28 The higher the compliance, the

larger the delivered volume per unit changes in pressure. Alveolar surface tension is an

important factor affecting the compliance of the lungs. If the surface tension is not kept low,

there is the inevitable tendency for the alveoli to collapse at smaller volumes during

expiration. Normally, the low alveolar surface tension is maintained at small alveoli volumes

due to the presence of pulmonary surfactant at the alveolar air-liquid interface. In contrast to

compliance, resistance describes the inherent capacity of the air conducting system and

tissues to oppose airflow towards the lungs.28

Airway resistance depends on the radii of the airways, the length of airways, the flow rate,

and the density and viscosity of gas. The airway resistance is inversely proportional to its

radius raised to the fourth power. Thus if the airway lumen is decreased by half, there is a

corresponding 16-fold increase in the airway resistance.28 Newborns and infants with their

inherently smaller airways are especially prone to marked increase in airway resistance from

inflamed tissues and secretions. This age-related difference in airway dimensions accounts

for why croup and bronchiolitis are almost entirely confined to infants and pre-school

children. Also, in patients with increased airway resistance (as is the case in bronchiolitis and

7

pneumonia), a fast respiratory rate does not allow enough pressure equilibration to occur

between the proximal segments of the airway and the alveoli, with a resulting tendency to

develop hypoxia.

Gas exchange: Gaseous exchange in the respiratory system occurs only in the terminal

segments of the airway via the process of diffusion and equilibration of alveolar gas with

pulmonary capillary blood (Figure 2). Diffusion depends on the expansive surface area of

the lungs (estimated to be approximately 160m2 in an adult) which promotes extensive

diffusion, and the amount of available time for equilibration.28 Also, the minute diffusion

distance of the thin alveolar and capillary walls (the alveolar-capillary barrier is less than

0.5 mm in thickness) enhances the rate of diffusion 28

Figure 2: Diffusion of gases across the alveolar–capillary membrane. (Image source- http://cuthbert7thgradescience.blogspot.com)

In health, the equilibration of alveolar gases and pulmonary capillary blood is complete for

both oxygen and carbon dioxide. In diseases in which alveolo-capillary barrier is abnormally

increased (alveolo-interstitial diseases) and/or when the time available for equilibration is

decreased (increased blood flow velocity), diffusion is incomplete.28

8

Oxygen transport: Oxygen (O2) diffuses through the respiratory membrane from the alveoli

to the blood from where it is transported to the tissues for utilization.28 The O2 is transported

in blood in two forms with majority bound to haemoglobin (oxygenated haemoglobin) and

the rest dissolved in plasma.28 The delivery of oxygen to a particular tissue depends on the

amount of O2 entering the lungs, the adequacy of pulmonary gaseous exchange, the blood

flow to the tissue, and the capacity of the blood to carry O2.28 Under normal conditions, each

100ml of blood contains about 20ml of oxygen bound to haemoglobin and about 0.3ml

dissolved in plasma.32 The dissolved fraction is available to tissues first, and then the fraction

bound to haemoglobin. Consequently as tissues metabolize oxygen or with inadequacy of

oxygen transport, the dissolved oxygen and the haemoglobin - bound oxygen will eventually

become depleted.32 In pneumonia, the oxygen transfer across the lungs and lung function

could become compromised as tissues continue to metabolize oxygen with a resultant

decrease in the percentage of oxygenated haemoglobin.

Control of respiration: The control and maintenance of normal breathing largely resides

within the bulbopontine region of the brainstem.28 The carotid bodies (peripheral

chemoreceptors) detect changes in partial pressures of oxygen (PaO2), carbon dioxide

(PaCO2) and pH, whereas the medullary (central) chemoreceptors monitor PaCO2 and pH

alone.28 The ventilatory drive is stimulated by PaO2 and PaCO2 levels, although the body

demonstrates far greater sensitivity to PaCO2 levels. In response to a decrease in pH, the

central chemoreceptors stimulate the respiratory center to increase the rate of inspiration.

Conversely, an increase in PaCO2 and/or a decrease in pH or PaO2, would each cause the

peripheral chemoreceptor to stimulate the respiratory center.28

Patho-physiology of respiratory signs in pneumonia: The arterial partial pressures of

oxygen (PaO2) and carbon dioxide (PaCO2) are tightly regulated by the central nervous

system, and therefore any alteration in their values can be taken as an indication that either

9

the regulatory system (the central control of breathing) or its effector organs (the respiratory

muscles and lungs) have become impaired or overwhelmed.33 Pneumonia may result in

hypoxaemia and respiratory failure from poor matching of pulmonary ventilation and

perfusion, or alveolar hypoventilation. This may occur following alterations in the

mechanical functions of the lung parenchyma, and usually manifest as a restrictive disease

with a corresponding decrease in the lung compliance. In the presence of this mechanical

dysfunction, arterial hypoxaemia and hypercapnia (and decreased pH) are sensed by the

peripheral and central chemoreceptors.33 After being integrated with other afferent

information from the lungs and chest wall, the activation of chemoreceptors trigger an

increase in the neural output to the respiratory muscles with the resultant physical signs that

characterize respiratory distress (Figure3 ).33

Figure 3: Pathophysiology of respiratory signs in pneumonia.33

Respiratory distress is a term utilized to summate a conglomerate of clinical features

reflecting respiratory ill-health.33 Features include tachypnoea, use of accessory muscles of

respiration like the intercostal muscles, lower chest wall indrawing, grunting, hypoxaemia

and cyanosis.33 The patient with respiratory distress develops a subjective perception of

difficulty in breathing or dyspnoea and consequently, an increase in respiratory muscle effort.

10

The physical signs of respiratory distress can be explained by a decrease in pleural pressure

during inspiration, recruitment of the accessory muscles that do not participate in normal

breathing at rest, and the activation of the dilator muscles of the upper airway as reflected by

a visible nasal flaring.33 Another prominent sign is grunting, which is due to decreased lower

airway compliance.33 The expiratory grunt is a physiological mechanism that generates high

pressure in the alveoli. The increase in intrapulmonary pressure at the initial phase of

grunting is associated with the closure of the glottis by the epiglottis during expiration.33

When the epiglottis subsequently opens abruptly, gas rushes past the vocal cords producing

the expiratory grunting sound. Thus, grunting is produced by expiration against a partially

closed glottis and is an attempt to maintain positive airway pressure during expiration for as

long as possible. Such prolongation of positive pressure is most beneficial in diseases that

produce widespread loss of the functional residual capacity, such as in extensive pneumonic

consolidation or one associated with pleural effusion.33 By maintaining a high intrapulmonary

pressure, more oxygen is expected to diffuse into the blood in the lungs. It is

characteristically seen in infants, and is a sign of severe respiratory difficulty. Disappearance

of grunting may suggest fatigue.33 End-organ hypoxia of the central nervous system causes

lethargy and confusion, sometimes alternating with agitation.33 The arterial hypoxaemia

causes haemoglobin desaturation, which if severe could manifest as central cyanosis.

HYPOXAEMIA

Hypoxaemia is generally defined as a decrease in the partial pressure of oxygen in arterial

blood.34 Specifically, it may also be defined as a partial pressure of oxygen in arterial blood

of less than 60 mmHg, or one causing haemoglobin oxygen saturation of less than 90%

recorded by pulse oximetry.32,34 On the other hand, hypoxia (which is sometimes confused

with hypoxaemia), refers to an abnormally low oxygen availability to the body, or an

11

individual tissue or organ. It may be defined as a state in which tissues receive an inadequate

supply of oxygen to support normal aerobic metabolism.34

Mechanisms of hypoxaemia

The mechanisms involved in the development of hypoxaemia include34:

1. Low inspired partial pressure of oxygen

2. Impairment of diffusion across blood-gas membrane

3. Alveolar hypoventilation

4. Shunt

5. Ventilation-perfusion inequality/mismatch

Conditions that result in hypoxaemia act via one or more of these primary mechanisms.

Low inspired oxygen partial pressure: If the partial pressure of oxygen in the inspired gas is

low, then a reduced amount of oxygen is delivered to the alveoli each minute.34 The reduced

oxygen partial pressure can be a result of reduced fractional oxygen content (low FiO2) or

simply a result of low barometric pressure as is the case at high altitudes. This reduced PiO2

can result in hypoxaemia even if the lungs are functioning normally. Furthermore, it is the

inspired oxygen content that is important in this case, rather than the atmospheric

concentration, as the person may not be breathing atmospheric gas (example is during general

anaesthesia).34 Low PiO2 is important in circumstances such as high altitude-induced

hypoxaemia (in which the FiO2 may even be normal). Hence, it may not be operative in

children with pneumonia-associated hypoxaemia.

Impaired diffusion: In health, the partial pressure of oxygen (PaO2) in capillary blood

equilibrates with the alveolar gas in approximately 0.25 seconds which is more than enough

time for adequate oxygenation of the red blood cell (RBC).34 This is because the RBC spends

0.75 seconds in the pulmonary capillaries. In disorders associated with a diffusion defect

such as interstitial fibrosis, interstitial processes retard the diffusion of oxygen into the

12

blood.34 Thus, such conditions associated with impaired diffusion across the blood-gas

membrane in the lungs may result in hypoxaemia.34 Although diffusion defects can be easily

corrected with the administration of supplemental oxygen, clinical conditions associated with

this defect are rare causes of hypoxaemia in paediatric practice.5

Alveolar hypoventilation: Alveolar ventilation is the volume of atmospheric air entering the

alveoli.34 The amount of alveolar ventilation per minute must be adequate to keep the

alveolar PO2 and PCO2 at values that will promote the escape of CO2 from venous blood, and

the uptake of oxygen by pulmonary capillary blood.5 Hypoventilation is defined as a PCO2

greater than 45mmHg and hyperventilation as a PCO2 less than 35mmHg.5 If the alveolar

ventilation is low, there may be insufficient oxygen delivered to the alveoli each minute. This

can cause hypoxaemia even in the absence of lung pathology, as the cause may be outside the

lungs. In a child with pneumonia, the occurrence of alveolar hypoventilation is ascribable to

extensive loss of functioning lung tissue.5

Shunt: This refers to blood that reaches the systemic circulation without coming into direct

contact with a ventilated area of the lung.5 This lowers the PO2 with a resultant hypoxaemia

because of the deoxygenated blood.5 Shunting of blood from the right side to the left side of

the circulation (right-to-left shunt) is a cause of hypoxaemia. Pathological shunts occur when

abnormal vascular channels exist, as is the case in cyanotic congenital heart disease.5 In the

diseased lung, shunting is most commonly associated with the continuing perfusion of the

unventilated alveoli. This is known as intra-pulmonary shunting. It occurs in a variety of

common paediatric clinical conditions such as pneumonia, pleural effusion (with or without

atelectasis).5

Ventilation-perfusion mismatch/inequality: The average ratio between alveolar ventilation

and blood flow (Va/Q) is 0.8, but even in normal lungs, this value may range from near zero

in the unventilated alveoli to infinity in the un-perfused alveoli.5 When a lung unit receives

13

inadequate ventilation relative to its blood flow, the PCO2 rises and the PO2 falls, with the

oxygen content of the end-capillary blood also falling.5 This blood mixes with blood coming

from normal Va/Q regions of the lung with the resultant lowering of oxygen concentration

and arterial hypoxaemia. This is the so-called “shunt-like” effect.5 Hypoxaemia by this

mechanism results from V/P mismatch emanating from areas of the lungs with ventilation

perfusion ratios that are less than one (but not zero).34 Clinically, ventilation/perfusion

mismatch is a major cause of hypoxaemia in children with pneumonia.5Administration of

supplemental oxygen will correct the hypoxaemia due to V/Q mismatch by raising the PO2.

This is in contrast to what happens in a true shunt. Thus, the administration of supplemental

100% oxygen allows differentiating between a V/Q mismatch and a shunt.5

Investigation of hypoxaemia

This can be achieved via:

the measurement of arterial blood gases(ABG),

the use of a pulse oximeter.

Analysis of arterial blood gases: Arterial blood gas (ABG) analysis refers to the

measurement the partial pressures of oxygen and carbon-dioxide, as well as the pH of arterial

blood.35 The values can then be used to assess how well the lungs are performing the function

of gas exchange and acid-base balance in the body. Direct measurement of arterial oxygen

tension using arterial blood gas sampling is very accurate. Compared with pulse oximetry,

arterial blood gas analysis remains the gold standard for detecting hypoxaemia.35 It is clearly

superior to pulse oximetry since unlike ABG, pulse oximetry does not measure the PCO2.32

However, ABG remains an invasive procedure requiring the potentially difficult arterial

puncture, hence the need for safer and less invasive methods like pulse oximetry.

Pulse oximetry: This is a non-invasive, simple, convenient and reproducible method of

measuring the haemoglobin oxygen saturation (SpO2).6,36 The equipment for this

14

measurement is referred to as a pulse oximeter. Pulse oximetry was first developed in

Germany in 1932 by Nikolai, Kramer and Matthes.32 While the early models of pulse

oximeters were designed using the spectrophotometric principle, modern pulse oximeters

combine the principles of optical plethysmography and spectrophotometry.32 The advent of

this modern variant of the equipment has been credited to the pioneering works of Aoyagi

and co-workers in 1974.37 Current models of pulse oximeter have a probe and an on-board

computer. The probe is made of two photo-diodes on one side and a photo-detector on the

other side of a pulsatile vascular bed such as the finger, toe, ear lobe or bridge of the nose.32

The use of this device requires no special training, thus providing an inexpensive early

warning of diminished tissue perfusion while avoiding the discomfort and risks of arterial

puncture. Appropriately tagged a ‘fifth paediatric vital sign’, the pulse oximeter has become a

reliable contemporary bedside tool for monitoring the level of hypoxaemia not only in

emergency paediatric practice, but also the intensive care setting.6, 36 By alerting the clinician

to the presence of hypoxaemia, the use of pulse oximeters can lead the health care worker to

an early recognition and treatment of severe hypoxemia. Thus, its use can prevent possible

serious complications.

Principles of pulse oximetry: This is based on two fundamental principles as detailed below.

The principle of spectrophotometry: This is based on the Beer-Lambert law which states that

the concentration of an unknown light-absorbing solute dissolved in a solvent can be

determined by the amount of light absorbed by that solvent.32 In respect of blood, the light-

absorbing solutes are oxygenated haemoglobin and deoxygenated haemoglobin. Thus, using

this principle, the percentages of oxygenated haemoglobin and deoxygenated haemoglobin in

the blood can be estimated.32 The two photodiodes used in pulse oximeters comprise one that

produces light at 660 nanometer (nm) in the red band of the spectrum, and another which

emits light at 900-940nm in the infrared band of the spectrum.32 These particular wavelengths

15

are used because the absorption characteristics of oxygenated-haemoglobin and

deoxygenated-haemoglobin differ at the two wavelengths; light emitted at 660nm is better

absorbed by oxygenated-haemoglobin, while light emitted at 940nm is better absorbed by

deoxygenated-haemoglobin.32

The principle of optical plethysmography: This is used to display the amplitude of the pulse

and heart rate. Each peak of the arterial waveform corresponds to one cardiac cycle.32 The

phasic signal presented to the sensor calculates the pulse amplitude according to the relative

absorption during systole and diastole.32 During ventricular systole, there is a phasic increase

of blood volume in the perfused organs, with light having to travel a longer distance through

distended subcutaneous tissue and a corresponding decrease in the light transmission through

the sampling site.32 During ventricular diastole, there is a phasic decrease of blood volume in

the perfused organs which results in light traveling a shorter distance through contracted

subcutaneous tissue, and the light transmission through the sampling site is increased.32 This

difference is used to generate a waveform which is displayed on the monitor (Figure 4).

Figure 4: Common pulsatile signals on a pulse oximeter32

A. Normal signal showing the sharp

waveform with a clear dicrotic notch.

B. Pulsatile signal during low perfusion

showing a typical sine wave.

C. Pulsatile signal with superimposed noise

artifact giving a jagged appearance.

D. Pulsatile signal during motion artifact

showing an erratic waveform.

16

Types of pulse oximeters

There are two types of pulse oximeter in contemporary use comprising the transmission and

reflectance pulse oximeters.32 Transmission pulse oximeters are however more commonly

used in contemporary clinical practice.

1. Transmission pulse oximeter: The components of this type comprise a pair of light

emitting diodes (LED) that emits light through interposed tissue (typically a finger, toe or

the ear lobe).32 The change in light frequency is read out by a photo-detector placed on

the opposite side of the interposed tissue.

2. Reflectance pulse oximeter: In this type, the photo-waves from the LED are bounced off

an appropriate surface such as the skull bone.32 The reflected light beam passes back

through the tissue to reach a photo-detector placed adjacent to the LED.

Procedure for using a pulse oximeter

The location for the probe is determined by the clinical situation and number of probes.32 A

re-usable probe makes the digits easily accessible. Apart from the digits, other sites include

the ear lobe, nasal bridge or septum, and the foot or palm of an infant.32 Tape or splints can

be used to secure the digit probe and minimize motion. After placement of the probe, the

equipment is switched on. The computer then analyzes the incoming data to identify the

arteriolar pulsation and displays this in beats per minute.32 Simultaneously, O2 saturation is

displayed on a beat-to-beat basis. In addition to the digital read-out of O2 saturation, some

devices display a plethysmographic waveform, which enables the user to distinguish an

artefactual signal from a true signal.32 If the oximeter fails to detect pulsatile flow, the

reading will either not be displayed, or depending on the machine, the SpO2 will be displayed

with a poor signal quality warning.32

Interpretation of readings: Patients with good gaseous exchange have SpO2 of 97% to

100%. When the SpO2 falls below 95%, hypoxaemia is present.32 SpO2 values of less than

17

90% represent relatively severe hypoxaemia.32 Children with SpO2 less than 92% often

require admission for oxygen and additional therapy.32 From the clinician’s perspective,

persistently low SpO2 values should be heeded as an important clinical warning sign.

Limitations of pulse oximetry

Specific limitations could be classified as technical or physiological, and whether they are

safe or potentially dangerous, as shown in Table I.36

Table I: Limitations of pulse oximeter.36

Safe Dangerous

Technical Mechanical artefacts

Electromagnetic interference

Magnetic resonance imaging

Accuracy

Calibration

Delay

‘Flooding’

‘Penumbra’

Physiological Pulse dependence

Volume

Rhythm

Abnormal haemoglobins

Other absorbents

Dyes

Delay

Pulsatile veins

Safe limitations may be defined as conditions when the pulse oximeter is not indicating the

correct value of SpO2, but the user is warned that the value may be inaccurate.36 On the other

hand, dangerous limitations are those where the device seems to be working correctly but

gives the wrong value.36 Details of these limitations of pulse oximetry are as provided below.

Mechanical artefacts are due to movement of the probe on the extremeties.36 Most pulse

oximeters are able to detect excessive movement and indicate malfunction, except the

movement is rhythmic and approximately at the heart rate. These artefacts are obvious if it

displays a plethysmograph wave.36

Electromagnetic interference (EMI) may cause a malfunction that is obvious if a trace is

displayed and always leads to an alarm situation.36 Common causes of EMI include the radio

frequency diathermy and the electromagnetic radiation from cellular phones.

18

Magnetic resonance image (MRI) is a special class of EMI.36 Due to the intense magnetic

field in the vicinity of MRI, metallic object should not be in the high field area.36 In order to

avoid this effect, special pulse oximeters containing both the LED and the photo-detector in

the case of the apparatus, are connected via optic fibres between the patient and the photo-

detector.36

Pulse dependence arises because pulse oximetry requires an adequate pulse volume.36 Most

pulse oximeters display a message indicating an inadequate pulse signal and thus such

readings could be discarded or the reading is taken only when an appropriate signal is

displayed.

Calibration of pulse oximeters are done against in vitro arterial blood samples tested in a co-

oximeter. This is a spectrophotometer that is dedicated to assessing haemoglobin oxygen

saturation.36 On the other hand, ABG values are derived from pH, carbon dioxide and oxygen

tension. Thus, pulse oximetry generated SpO2 should never be compared with values

indicated by blood gas analysis for calibration.

Accuracy of pulse oximeters is quoted by most manufacturers of being +/- 2%.36 Strictly,

pulse oximeters indicate neither functional nor fractional O2 saturation values. Indeed, the

pulse oximeter O2 saturation is the value of O2 saturation using the wavelength of 660nm and

940nm. For this reason, the abbreviation SpO2 should always be used for pulse oximeter

generated oxygen saturation values.

Delay may occur between a change in O2 saturation and a corresponding change in pulse

oximeter reading.36 These delays may be attributed to irregular pulse volume or rhythm

slowing the computation of SpO2.36

It may also be ascribed to averaging algorithms which

produce more accurate but slower readings.36 When using the SpO2 to detect hypoxaemia,

separate measurement systems to differentiate between an alarm for inspired oxygen

concentration and failure/disconnection of mechanical ventilation should be used.36 This is

19

important to prevent a comparatively late warning. Placement of the probe centrally (cheeks

or tongue) rather than peripheral may halve the delay in oximeter display of values

suggesting desaturation.36

Flooding occurs when extraneous energy sources especially bright visible or infrared light

overload the semiconductor detector.36 If the pulse oximeter does not give an alarm to

indicate flooding, it may display a reading of 85%. This is because a ratio of red/infrared of

one is equivalent to a SpO2 of 85%. A similar problem, penumbra effect, often occurs in

children.36 In this case, the pulse oximeter may over-read or under-read due to the existence

of a different path length of tissue for each of the wavelengths.36 This occurs with very small

fingers or when the LED is projected tangentially through the tip of a digit. To avoid this

effect, probes designed for children should be used.

Current pulse oximeters are unable to detect dyshaemoglobins, and will therefore produce

erroneous results.36 For example, carboxyhaemoglobin and methaemoglobin levels can cause

the pulse oximeter to over-read. If significant levels of these dyshaemoglobins are

anticipated, the use of a co-oximeter is preferred.36 Co-oximeters are safe to use in the

presence of abnormal haemoglobin, as one machine uses as many as 17 wavelengths, unlike

the pulse oximeter which uses two wavelengths.

Dyes given intravenously such as methylene blue, indocyanine green and indigo carmine can

cause falsely low SpO2 readings, an effect that persists for up to 20 minutes.36 The accuracy

however improves as the dye dilutes.

Anaemia, when severe, causes the pulse oximeter to become less accurate and less reliable as

the device depends on light absorption by haemoglobin. Accuracy is however, not diminished

until the haemoglobin content is less than 5g/dl.36 This should be taken into consideration

when taking pulse oximeter readings in children with haematocrit values of less than 15%.

20

Skin pigmentation and other pigments may be associated with inaccurate oximetry readings.36

Placing the probe on the fifth finger or an earlobe has been suggested as a means of

minimizing this effect.

Indications/ clinical applications of pulse oximetry

i. Detection of hypoxemia: With the introduction of pulse oximetry, hypoxemia is

detected earlier and more often in critically ill patients.38 The current study used the

pulse oximeter to detect hypoxaemia in children with pneumonia.

ii. During emergency airway management: The pulse oximetry is useful in this instance

to assess whether there is need for further airway management, and also to assess the

adequacy of pre-oxygenation before endotracheal intubation.38 It is also an invaluable

tool for monitoring ventilator changes, providing an early index of ventilator

dysfunction and the need for weaning the patient off oxygen therapy.38

iii. Titration of fractional inspired oxygen concentration (FiO2): Pulse oximetry can assist

with titration of FiO2 in ventilator-dependent patients.38

iv. In acute asthma: Pulse oximetry has been evaluated as a means of screening for

respiratory failure in patients with acute severe asthma with or without life threatening

features.38

v. Oxygenation monitor: The pulse oximeter may also serve as a sensitive monitoring

device to detect a sudden drop in oxygenation during procedures involving sedation,

inter-hospital and intra-hospital transfer.38 It is also a useful adjunct in deciding the

desirability and progress of weaning a patient off oxygen.38

Pneumonia

Pneumonia refers to a disease of the lungs caused by micro-organisms in which there is

accumulation of secretions and inflammatory cells in the pulmonary alveolar spaces.39

Essentially, it can be broadly defined as a pathogen-driven inflammation of the lung tissue

21

resulting in damage to the lung tissue.40 Different definitions for pneumonia exist, varying

from the microbiologic identification of pathogens in lung specimens, to the radiologic

presence of pulmonary infiltrates in chest radiographs, or one based solely on the clinical

findings of tachypnoea or chest retractions.40 The World Health Organization (WHO)

guidelines define pneumonia as an acute disease episode with cough and/or difficult

breathing, associated with respiratory rates exceeding the age-specific cut-off values.41 This

WHO operational definition has proved useful worldwide for early disease identification in

facilities without access to chest radiography. For practical and conventional reasons, most

respiratory physicians define pneumonia as a lower respiratory illness associated with the

relevant clinical findings like fever, breathlessness/difficulty breathing, tachypnoea,

auscultatory features of consolidation and/or crepitations, and the corroborative evidence of

radiographic infiltrates on chest x-ray.40

Classification of pneumonia

Pneumonia may be classified in various ways, but the following constitute the common basis

for categorizing the disease in children:

I. Area of probable origin: This includes community-acquired pneumonia (CAP) which

is defined as pneumonia acquired outside the hospital setting, or hospital acquired

(nosocomial or health-care associated infection) pneumonia.39 The latter type refers to

pneumonia which has its onset during a stay in the hospital, and up to one week after

discharge.

II. Pattern of involvement/anatomical distribution: This is the basis for the common

categorization as lobar-, broncho-, and interstitial pneumonia.39 In lobar pneumonia,

most of the parenchyma within an anatomic lobe is affected, sparing the airways with

a positive air bronchogram sign on chest radiograph.39 On the other hand,

bronchopneumonia is characterized by multiple, patchy opacities, usually bilateral.

22

Interstitial pneumonia is associated with streaky opacities with an interstitial

distribution.39

III. The type of infecting micro-organism: These include bacterial, viral, mycoplasmal,

chlamydia, and fungal pneumonia.39 The pathogen-based classification can also be

based on the actual infecting organism such as staphylococcal, streptococcal,

Haemophilus influenzae, tuberculous, parainfluenza, adenoviral pneumonia or

pneumocystic jiroveci pneumonia associated with HIV/AIDS.

Epidemiology of pneumonia

A recent review of the epidemiology of pneumonia has shown that the estimated median

incidence of pneumonia for developing countries is 0.28 episodes per child-year, with an

inter-quartile range of 0.21–0.71 episodes per child-year in under-five children.2 This equates

to 151.8 million new cases every year, 13.1 million or 8.7% (7–13%) of which are severe

enough to require hospitalization.2 More than half of the world’s annual new cases of

pneumonia are concentrated in six countries where 44% of the world’s children aged less

than five years live. These countries comprise India, China, Pakistan, Bangladesh, Indonesia

and Nigeria.2 In Nigeria, the estimated median incidence was 0.34 episodes per child-year,

with an inter-quartile range of 0.31-0.40 episodes per child-year.2 This equates to 6.1million

new cases each year in under-five children.2 A previous study from Ilorin, Nigeria reported a

mean pneumonia incidence value of 1.3 episodes per child-year.3

Recent estimates of the total pneumonia-related mortality by the Child Health Epidemiology

Reference Group (CHERG) indicate that there are more than two million deaths due to

pneumonia each year in children aged less than five years.2 These estimates are exclusive of

deaths in the neonatal period, 26% of which are related to severe infections, including

pneumonia.42 Additionally, at least another 300,000 deaths caused by pneumonia are likely to

occur worldwide during the neonatal period.42

23

Pneumonia-related deaths vary widely between the major WHO regions and increases

significantly in relative importance in regions that have inefficient health systems.2 In

general, the African region has the highest burden of global child mortality.2 This region,

inhabited by about 20% of the world’s population of children aged less than five years, has a

disproportionate 45% of all deaths occurring globally in the same age group and 50% of such

deaths have been ascribed to pneumonia.2 By contrast, less than two percent of these deaths

take place in the same age group in countries of the European region, while less than three

percent occur in North America.2 Indeed two-thirds of these pneumonia-related deaths are

concentrated in just 10 countries, of which India, Nigeria, the Democratic Republic of the

Congo, Ethiopia and Pakistan rank as the top five.2 In Nigeria, the estimated (national)

mortality rate is 84.7/10,000 in under-five children.2 Earlier studies from the South West

(Ibadan) and North central (Ilorin) had reported the case fatality rates of 7.8 and 10% in

under-five children with pneumonia.3,4,43

Risk factors of pneumonia

Various risk factors of pneumonia associated morbidity and mortality have been identified

and can be categorized as demographic, socioeconomic, environmental, nutritional and co-

morbid risk factors.

A. Demographic risk factors: These include

Age: Pneumonias are common in infancy with a stepwise decrease in the age-specific

incidence with increasing age.44 Also, a fatal disease outcome is generally more likely in

the younger child.44

Gender: There is a male preponderance for the incidence and prevalence of pneumonia.44,

45 Whereas boys may appear more frequently affected by pneumonia than girls, this may

be partly ascribed to the confounding effect of a possible gender bias regarding health

seeking behaviour in many communities.44

24

B. Socio-economic risk factors: These may be sub-categorized as follows:

Family income: The first indication that pneumonia is associated with socioeconomic

factors is the pronounced differences between industrialized countries and those of the

developing world.44 The estimated incidence of pneumonia in children aged less than 5

years was 0.29 and 0.05 episodes per child-year in developing and industrialized countries

respectively. This translates to 151 million and 5 million new episodes respectively each

year.2 Furthermore, the annual incidence of pneumonia which ranges from 3% to 4% in

industrialized countries and 10% to 20% in developing countries constitutes yet another

evidence of the negative impact of poverty on the incidence of pneumonia.2

Parental education: A 2011 review of various studies done by Principi and Esposito on

pneumonia in developing and developed countries reported that poor maternal education

was associated with an increased risk of hospitalizations and mortality due to

pneumonia.46

C. Environmental risk factors: The most frequently studied environmental risk factors for

respiratory infections include exposure to environmental pollutants and crowding.

Atmospheric pollution: Refers to introduction into the air of any substance different from

any of its natural constituents.47 This may come from one or more of noxious atmospheric

gases (such as carbon monoxide, sulphur dioxide, benzene and ozone) or particulates like

dust or soot from several domestic sources.47 These pollutants can cause impairment of the

natural respiratory defense mechanisms if inhaled at adequate concentrations, and over a

long enough period of time. Some earlier Nigerian reports had identified an association

between air pollution levels and respiratory illnesses.22, 47

Domestic biomass pollution: In Nigeria, as is the case in many tropical countries, cooking

is often done indoors in poorly ventilated rooms with the possibility of a consequent build

up of high levels of domestic smoke pollution.22 Studies have shown that the occurrence of

25

pneumonia increases in direct relation to the amount of time a child spends exposed to this

type of pollution.21,48 In Nigeria, and many other tropical African communities, young

infants are usually carried on the backs of mothers while cooking. This puts such infants at

special risk of culinary smoke exposure.21,22

Environmental tobacco smoke: The association between environmental tobacco smoke,

often referred to as passive smoking, and respiratory illness in childhood has been

established by some earlier studies.49,50 In a cohort of children followed up for the first two

years of life in Brazil, Victora et al51 found a 50% increase in ALRI hospitalizations

among children with two smoking parents compared to children of non-smokers. This

association is reportedly stronger for infants than for older children, and also stronger for

maternal smoking than for paternal smoking.49,50

Crowding: This occurs in various forms such as the number of siblings in the household,

room occupancy, population density, as well as daycare attendance. Crowding, a common

occurrence in most developing countries, was found to contribute to the transmission of

droplet-acquired respiratory infections.44 Crowding-related variables such as birth order

and the number of children under-five years in the household have been associated with a

higher risk of pneumonia.2,44,49,52 Of a cohort of 238 children who attended day care during

the first year of life, Celadon and others reported that children who attended day care

were 1.6 times more likely to have ALRI compared with those not attending day care.53

D. Nutritional factors: The nutrition-related factors that may influence the risk of

pneumonia include birth weight, breast-feeding, the nutritional (macronutrient) status, as

well as the levels of vitamin A and zinc.2

Malnutrition: Most hospital-based data found a two- to four- fold increase in the

prevalence of pneumonia among malnourished children.24,44,45,52 In a systematic review of

16 relevant studies in developing countries, Chisti et al52 reported that children with

26

pneumonia and moderate or severe malnutrition (defined as <-2 to ≥-3 z- score of weight-

for-age, weight-for-height or 60–74% weight-for-age of the median of the NCHS) are at

higher risk of death. Improving the nutritional status of children is therefore a potentially

beneficial intervention towards preventing pneumonia, reducing the associated mortality,

as well as improving growth and development in children in the developing countries.19

Breast-feeding: Breast milk may protect against pneumonia through a number of

mechanisms, which include its contents of antibacterial and antiviral substances,

immunologically active cells and stimulants of the infant’s immune system.26 Also, studies

concerning the association between breast-feeding and overall infant mortality in

developing countries suggest a protective effect of exclusive breast-feeding in early

infancy.2, 19, 26 Not only was pneumonia common in those who were not breast-fed, but

pneumonia-related deaths were reportedly higher in the same group.2,19,26,54

Micronutrient deficiency: The two micronutrients that have been identified to have a

major impact on the morbidity and mortality burden of pneumonia in children include

Vitamin A and zinc.

o Vitamin A: Vitamin A, a fat-soluble vitamin which is available in liver and dairy products,

is known to enhance immune function and also plays an important role in the normal

functioning of the lungs, skin, intestines and eyes.55 Unlike most risk factors for

pneumonia, the evidence on the role of vitamin A deficiency results mainly from

randomized controlled trials.55,56 Periodic vitamin A supplementation in children was

shown to substantially reduce the overall childhood mortality.55 Furthermore, a large-dose

vitamin A supplementation during illness has been shown to reduce the mortality, severity

of illness, and the duration of pneumonia in children with measles.56

o Zinc: Zinc is an essential nutrient and factor for the immune system.57 Zinc deficiency

decreases the ability of the body to respond to infection, and it is also known to affect

27

adversely both cell-mediated and humoral immune responses.57 The evidence of the

importance of zinc in child health has come from recent randomized controlled trials of

zinc supplementation. A systematic review of studies evaluating preventive effects of zinc

supplementation on the morbidity burden of ALRI noted an overall reduction of 15% in

the incidence of pneumonia in zinc-supplemented preschool children.58

E. Co-Morbid factors/Inter-current illness: These include conditions such as diarrhoea

disease, measles, pertussis and concomitant infection with the Human Immunodeficiency

Virus/ Acquired Immunodeficiency Syndrome (HIV/AIDS).

Diarrhoea disease: It has been shown that children who suffer from repeated or severe

episodes of diarrhoea are also at a higher risk of pneumonia.27,59,60 However, it is not clear

whether these conditions are causally related or whether their observed co-occurrence

merely reflects the presence of common risk factors, for example a weak immune system

and malnutrition. The latter view is supported by the fact that risk factors such as lack of

breastfeeding, low family income and age are commonly identified in children with

diarrhoea disease, as well as those with pneumonia.2 Diarrhoea may also increase the risk

of pneumonia in the short term by causing acute micronutrient loss, stressing the host

immune system, causing dehydration and consequently creating a vulnerable period of

increased risk of infections. Recently, a review of studies carried out in Ghana and Brazil

were compared to see the association between pneumonia and diarrhoea.27 In the review,

diarrhoea disease contributed substantially to the risk of pneumonia within a few weeks of

its occurrence.27

HIV/AIDS: The HIV pandemic has had a great impact on childhood mortality in sub-

Saharan Africa since 1990.23 In addition to the increased predisposition of HIV-infected

children to bacterial and viral (non-HIV) pneumonia, HIV-infected children have also

been found to have a 6.5 times greater case-fatality rate than HIV-uninfected children.61

28

Measles and pertussis: Measles is a major cause of ALRI in developing countries.62

Hospital and community-based studies of pneumonia have found that measles accounted

for 6%-21% of the morbidity and 8%-93% of the pneumonia-related mortality.62

Furthermore, measles and pertussis are commonly complicated by pneumonia, while co-

morbid measles or pertussis in children with pneumonia is associated with a severe disease

and higher case-fatality.2,43,52,62

Aetiological agents of pneumonia

There is a wide spectrum of potential causative agents of pneumonia, but the major categories

comprise bacterial and non-bacterial pathogens. These may be specific viral, bacterial, fungal

or mycoplasmal agents.40,46 Studies have shown that mild and moderate CAP is mainly

caused by viruses, particularly in the first year of life, whereas most cases of severe CAP are

caused by bacteria.2,49,52 However, it has also been shown in developing and developed

countries that measles virus, influenza viruses and respiratory syncytial virus play a major

role in causing severe and/or complicated CAP.43,45,63 The leading bacterial cause in several

earlier studies was Streptococcus pneumoniae (pneumococcus) reportedly identified in 30.0–

50.0% of pneumonia cases.46,64-68 The second most common organism isolated in most

studies was Haemophilus influenzae type b (Hib; 10.0–30.0% of cases) followed by

Staphylococcus aureus and Klebsiella pneumonia in the paediatric pneumonia cases.46, 64-68

However in the studies by Johnson et al and Fagbule et al, from Ibadan and Ilorin in the

South West and North Central regions of Nigeria respectively, Staphlococcus aureus was

identified to be the commonest bacterial agent.45,69 The importance of ‘atypical’ bacteria

(Mycoplasma pneumoniae and Chlamydia pneumoniae) in severe and/or complicated CAP

has not been completely defined worldwide, largely because of difficulties in identifying

them.67 However, recently published data indicate that a considerable number of children

with CAP caused by atypical bacteria would have a complicated course, mainly because of

29

the presence of pleural effusion.70 The causative agent of pneumonia has been found to differ

according to the age of the patient as shown in Table II.40

Table II: Common agents causing community-acquired pneumonia according to age. 40

Age

Newborns 1 – 3 months 1 - 12 months 1 – 5 years Older than 5 years

Enteric Gram

negative, Group

B streptococcus

Viruses,

Chlamydia

trachomatis,

Ureaplasma

urealyticum,

Bordetella

pertussis

Viruses,

Streptococcus

pneumoniae,

Haemophilus

influenzae,

Staphylococcus

aureus,

Moraxella

catarrhalis

Viruses,

Streptococcus

pneumoniae,

Chlamydia

trachomatis,

Mycoplasma

pneumoniae

Streptococcus

pneumoniae,

Mycoplasma

pneumoniae,

Chlamydia

pneumoniae

In recent years, the HIV pandemic has also contributed substantially to increases in the

incidence and mortality from childhood pneumonia.2 In children with HIV, CAP remains a

major cause of mortality, but additional pathogens like Pneumocystis jiroveci have also been

found in HIV-infected children.2 Other organisms such as Mycoplasma pneumoniae,

Chlamydia spp, Pseudomonas spp, Escherichia coli, measles, varicella, influenza,

Histoplasma capsulatum and Toxoplasma gondii can also cause pneumonia in children with

HIV.2

Clinical features of pneumonia

The major clinical manifestations of pneumonia include fever, cough, tachypnoea,

breathlessness/difficulty breathing, poor feeding/anorexia, and in the older child capable of

complaining, chest pain.40 The presence of restlessness and/or cyanosis may suggest

hypoxia, while vomiting and diarrhoea are particular symptoms prominent in infants.40

Children with pneumonia may also present with abdominal pain and/or vomiting and

headache. Among other physical signs, children with pneumonia may have chest wall

retractions, the presence of bronchial breath sounds and/or crepitations on auscultation.40 In

the overtly malnourished or immunocompromised child with pneumonia, respiratory signs or

30

symptoms are notably few. Using the age-specific cut-off points as the reference points,

tachypnoea has been identified as an invaluable sign of pneumonia in developing countries.71

Some earlier reports have however contended that respiratory rate may not be particularly

useful in identifying children with pneumonia, especially in the infant.72,73

Using clinical and radiological parameters two major types of pneumonia can be

distinguished as lobar and bronchopneumonia.4,24,74 In bronchopneumonia, patchy opacities

of the lung field on chest radiograph, auscultatory findings of diminished breath sounds and

coarse crepitations constitute the usual characteristics.4,24,74 On the other hand, lobar

pneumonia is characterized by reduced chest movement on the affected side, dullness to

percussion, bronchial or tubular breath sounds and crepitations. In addition, a homogenous

opacity involving the affected lobe with or without a positive air bronchogram sign is usually

evident on the chest radiograph in lobar pneumonia.4,65

Complications of pneumonia

Various complications of pneumonia have been reported. Heart failure has been reported as

the most common in most studies.4,24,45,74 Respiratory complications reported include pleural

effusion, empyema, pneumothorax, subcutaneous emphysema, lung abscess, pneumatocoeles

and purulent otitis media.4,24,45,74 Other complications reported were anaemia, gastroenteritis,

pericarditis and septicaemia.4, 24

Investigations in pneumonia

The goals of investigations are to confirm a diagnosis and exclude the close differential

diagnoses. Furthermore, investigations may also be carried out to determine the causative

organism, the extent of the lesion present as well as to monitor the response to management.

Investigations may be specific or supportive. For pneumonia, these include radiological,

microbiological and haematological investigations.

31

Radiological: Chest radiography remains perhaps the most frequently requested investigation

in confirming a diagnosis of pneumonia.40 A posterior-anterior (PA) film, with or without a

lateral, is often used. Radiographic findings of pneumonia include peribronchial and

interstitial infiltrates, or lobar/segmental consolidation with the air bronchogram sign.4,46,49,74

A chest radiograph is also useful in identifying the anatomic pattern of the parenchymal

lesion, location, extent and/or the presence of associated intrathoracic lesions/complications

such as hyperinflation, parapneumonic effusion and air-leak syndromes.39,46 In addition to

aiding diagnosis, chest radiographs are also useful in monitoring the course of pneumonia.39,

46 Also, certain radiographic patterns may suggest the possibility of a specific aetiology. A

right upper lobe consolidation with bulging fissure may suggest Klebsiella pneumonia while

the presence of pneumatocoele, with or without pleural effusion may suggest a

Staphylococcal aetiology.39 Perihilar infiltrates in a previously healthy infant may suggest a

possible viral aetiology.

One of the problems about interpreting chest radiographs is the great intra- and inter-observer

variation in radiographic features used for diagnosing pneumonia, and also the lack of

standardization. The WHO produced a method for standardizing the interpretation of chest

radiographs in children for epidemiologic purposes.75

Microbiological: Investigative tools under this category are particularly useful in identifying

the aetiological agent of pneumonia. Whereas the identification of the causative pathogen

enables the health worker to select the appropriate antimicrobial agent, the ideal investigative

tool for identifying most pathogens of pneumonia remains elusive. Some of the methods

available for detecting the aetiological agent(s) of pneumonia include:

Nasal wash or nasopharyngeal swab: These samples have been used for viral detection by

culture, polymerase chain reaction and/or immunofluorescence. Swab samples may be used

to detect some bacteria agents such as Streptococcus pneumoniae and Hib.45, 66 It is however

32

important to note that the identification of bacterial growth from the nasopharynx does not

indicate infection in the lower airways.

Blood culture: A sample obtained before the commencement of antibiotics has been

identified as a specific investigative tool for pneumonia, with a positive yield correctly

identifying the causative organism in 20-33% of patients in different studies.45,46,65,66 69

Pleural fluid culture: This may grow potential pathogens, but the usual practice of empirical

antibiotic use in pneumonia may reduce the sensitivity of this method.76 However, pleural

fluid should be aspirated for microscopic examination and culture whenever technically

feasible.76

Sputum culture: Children aged less than ten years are unable to produce adequate sputum. 76

Furthermore, samples are usually contaminated by oral flora. Induced sputum production,

with the use of nebulized saline, has been used in children aged less than five years not

capable of producing sputum.66

Bronchoscopy: Flexible fiberoptic bronchoscopy has been useful to obtain lower air way

secretions for culture or cytology.76 Samples that can be obtained by bronchoscopy include

bronchial washings, bronchoalveolar lavage fluid and transbronchial biopsy specimens.76

Lung aspirate: Lung aspirate studies have been used in several earlier studies to identify the

common bacterial agents of pneumonia in childhood.65,66,69,77,78 The reported diagnostic yield

from culture of lung aspirates is approximately 50% in children, as opposed to the yield of

20%- 30% from blood culture.78 The reported complications include pneumothorax in 1.5-9%

of cases and a transient small haemoptysis identified in 0.7-3% cases.65,66, 69, 77,78

Serology: The demonstration of a four-fold rise in the titres of specific antibody to the target

pathogen(s) in the two serum samples taken 10-14 days apart, at the acute and convalescent

phases, is considered a sufficient ground for a recent infection due to the pathogen(s).45, 79

33

Serology is an invaluable laboratory tool for detecting viruses, chlamydial and mycoplasmal

organisms.39,45,79

Nucleic acid amplification tests: These tests have been developed by many modern

laboratories to achieve a rapid and accurate detection of those pathogens that are difficult to

culture.76 One of such tests is the polymerase chain reaction (PCR) assay, which may be

applied to specimens from respiratory secretions, lung aspirate samples or blood.76 Viruses,

M. pneumoniae, C. pneumoniae, and bacteria agents can be identified through this method. It

has excellent sensitivity and specificity for pathogen identification, but is costly and time-

consuming. Furthermore, its usefulness is also limited by the inability to differentiate a

carrier state from an active disease except for lung aspirate studies. The cost of the equipment

continues to underscore the poor availability of this method in most developing countries.

Other tests: These includes hematological and blood biochemistry tests.

Haematological: This test provides only supportive clues of a current infection. A complete

blood count (CBC) may show anaemia with leucocytosis in an infant with Staphylococcal

pneumonia.39 Also, leucocytosis with a left shift in the presence of pneumonia would suggest

a bacterial rather than viral origin.39

Blood biochemistry and arterial blood gas determination: These tests are considered useful in

monitoring the response to fluid therapy and supportive care. This is necessary in view of the

risk of hypoxaemia, respiratory failure and syndrome of inappropriate antidiuretic hormone

secretion (SIADH).39

An overview of hypoxaemia and pneumonia

Hypoxaemia constitutes a serious manifestation of severe respiratory illness. Indeed, it is a

strong risk factor of ALRI-related mortality, particularly pneumonia.7,8,80,81 Several co-

morbidities and respiratory complications may follow pneumonia. While the common

respiratory complications of pneumonia include atelectasis, pleural effusion and acute

34

respiratory failure amongst others, systemic consequences also abound. A systemic

complication of many lower respiratory infections is hypoxaemia. Pneumonia-related

hypoxaemia can evolve from more than one mechanism.5 The presence of alveolar

hypoventilation in pneumonia may occur due to extensive loss of lung tissue, as is the case in

those with associated atelectasis. On the other hand, hypoxaemia may complicate pneumonia

from the associated limitation of chest wall movement, as is the case with an associated

pneumothorax or pleural effusion.5 In addition, pneumonia-related intrapulmonary shunting

and ventilation-perfusion mismatch may also lead to hypoxaemia, and ultimately respiratory

failure.

A systematic review by Lozano82 reported that the prevalence of hypoxaemia in children with

ALRI using pulse oximetry varied from 6-8% in the outpatient setting, increasing to 31%

and 43% in emergency room patients and those with clinical pneumonia respectively. Also,

the prevalence was reportedly higher among hospitalised children (47%) and in those with

radiographically confirmed pneumonia (72%).82 However, the differences in the criteria for

establishing the diagnosis of pneumonia and bronchiolitis was not mentioned in several

reports included in the review by Lozano. Also, some reports with lower prevalence values of

hypoxaemia studied ambulatory and hospitalised children with several forms of ALRI.9,10

In a more recent literature review in 2009, the corresponding median prevalence of

hypoxaemia associated with WHO-defined pneumonia was estimated as 13% in the

developing countries.7 While there is evidence that the prevalence of hypoxaemia in

hospitalized children with pneumonia differs between regions, the differences are however

within comparable pneumonia severity classifications and heights above sea level. However,

the reported prevalence is consistently lower in reports emanating from Africa (eight studies;

range of prevalence 3–10%) compared with those from Asia (eight studies; range of

prevalence 9–39%). In addition, the prevalence of pneumonia-associated hypoxaemia from

35

locations that are more than 1000m above sea level,16,83,84 ranged from 39% (for a study

based on WHO-defined pneumonia)16 to 73% (for a study in which the diagnosis was based

on radiographic findings).83

Traditionally, the monitoring of hypoxaemia in the patient with pneumonia has been with

arterial blood gases. More recently however, pulse oximetry has been identified as a more

convenient, safer and valid monitoring tool. The severity of hypoxaemia is affected by

altitude, haematocrit concentration, degree of acidosis, and the body temperature all of which

are important considerations in determining the oxygen-carrying capacity of blood.32 As a

non-invasive, simple and reproducible method of measuring the oxygen saturation of arterial

haemoglobin, pulse oximetry remains a reliable bedside tool for monitoring the level of

hypoxaemia in paediatric practice.6 However, the required pulse oximeters are relatively

expensive and have the additional recurring costs of the need for replacing the probes. For

these reasons, they are not usually available in most primary health care facilities and even in

many referral facilities in developing countries.

While pneumonia may be diagnosed by identifying tachypnoea, with or without chest wall

indrawing, the clinical recognition of hypoxemia is more problematic. Different sets of

clinical signs and symptoms have been studied to predict the presence of hypoxemia in

children with pneumonia.13 Majority of such studies were carried out at high altitude,8,80,82-86

as against the limited data from locations at sea level.13 Therefore, in order to guide the health

care worker regarding the desirable timing of appropriate intervention like oxygen therapy or

referral, the early detection of these clinical clues of hypoxemia will be a crucial part in the

clinical management of patients with pneumonia. Such clinical symptoms and signs like

altered levels of consciousness are often attributable to compensatory respiratory responses to

hypoxaemia, or indeed, the clinical indicators of its consequences.

36

The major physical signs attributable to hypoxaemia include central cyanosis, tachypnoea,

chest wall retractions, and the use of accessory muscles of respiration, sometimes resulting in

head nodding. Central cyanosis, which sometimes poses some difficulties in the black race,

was reportedly highly specific (with a range of 84-100%) but the corresponding sensitivity is

poor (9-42%).8-11,14 The clinical interpretation of this is that although the presence of central

cyanosis is useful for identifying hypoxaemia, inability to detect its presence does not

exclude hypoxaemia. On the other hand, against the background of a reported sensitivity and

specificity of 82% and 51% respectively, respiratory rates above the age-specific cut-offs

remains perhaps, the single most useful clinical sign for predicting hypoxaemia.17 Inability to

drink/feed and altered mental state (which encompasses severe lethargy, prostration, or

sometimes coma) was reported to have a sensitivity of less than 50% and an equally poor

specificity in most studies.8, 84 Other clinical signs like chest wall indrawing and grunting

though specific for hypoxaemia (83%) had a modest sensitivity(69%).16 Also, the specificity

of 83% and sensitivity of 57% associated with head nodding were comparable to those of

chest wall indrawing and grunting. The poor predictive value of auscultatory finding of either

rhonchi or crepitations is indicated by the reported poor specificity of 47% at high altitude,

despite a corresponding sensitivity of 96%.16,17

Whereas several risk factors of pneumonia have been previously studied, especially with

respect to pneumonia-related mortality,2 54 to the best knowledge of this researcher, the

relationship between these risk factors and the presence of hypoxaemia has hardly been

earlier explored. Studies have shown that the risk of hypoxaemia was between 3.5 to 16.2

times higher in the presence of pneumonia than in the more common acute upper respiratory

illnesses.17, 87 In addition, the relative risk of mortality in children with hypoxaemic

pneumonia is notably higher than in those with non-hypoxaemic pneumonia at

admission.8,10,12 Furthermore, hypoxaemia is associated with a two-to five-fold increase in the

37

risk of a fatal outcome from pneumonia.8,10,12,80 Also haemoglobin oxygen saturation (SpO2)

measured using a pulse oximeter has been shown to correlate with the outcome of pneumonia

in children.86 The management import of these observations is that if a fatal outcome is to be

avoided in children with pneumonia, it is important to detect hypoxemia as early as possible

with a view to effecting the appropriate modifications of the initial treatment strategies.

In conclusion, it can be surmised that hypoxaemia had earlier been overlooked in worldwide

strategies for pneumonia control and reducing child mortality. Worse still, the import of this

complication has also been frequently underestimated in developing countries, apparently due

to the limited availability of the required hypoxaemia-monitoring tools like ABG facilities

and pulse oximetry.7 Yet, the accurate identification of hypoxaemia in pneumonia will be

crucial in determining the safety or otherwise of continuing outpatient treatment, or indeed,

may constitute a valid criterion for possible hospital admission. There is thus a need for more

data on the prevalence of hypoxaemia amongst children with pneumonia, as well as the

profile of children who are hypoxaemic, and those who are potential beneficiaries of prompt

oxygen treatment.

Management of pneumonia

The main principles in the management of pneumonia are to assess disease severity, eradicate

the infection, give symptomatic care and deal with complications.

Severity assessment: The spectrum of severity of pneumonia can be mild to severe using the

British Thoracic Society guidelines (Table III).88 The presence of any of the signs of severe

pneumonia is an indication for hospital admission. Infants and children with mild to moderate

respiratory symptoms can be managed safely in the community.88 The severity assessment

will also influence microbiological investigations, initial antimicrobial therapy, routes of

administration, duration of treatment and level of nursing and medical care.

38

Table III: British Thoracic society severity assessment of pneumonia88

Mild to moderate Severe

Infants Temperature <38.5°C Temperature >38.5°C

RR <50 breaths/min RR >70 breaths/min

Mild recession Moderate to severe recession

Taking full feeds Nasal flaring

Cyanosis

Intermittent apnoea

Grunting respiration

Not feeding

Tachycardia(age dependent)

Capillary refill time > 2seconds

SpO2<92%

Older Children Temperature <38.5°C Temperature >38.5°C

RR <50 breaths/min RR >50 breaths/min

Mild breathlessness Severe difficulty in breathing

No vomiting Nasal flaring

Cyanosis

Grunting respiration

Signs of dehydration

Tachycardia (age dependent)

Capillary refill time > 2 seconds

SpO2<92%

On the other hand, using the WHO classification for severity, pneumonia could be assessed to

be non-severe, severe and very severe.41 The presence of cough or difficult breathing plus

age-specific increase in respiratory rate (>60 breaths/min for infants aged less than two

months, >50 breaths/min for infants aged two months up to less than 12 months, and >40

breaths/min for children aged 12-59 months) is classified as non-severe. Severe pneumonia is

diagnosed when in addition to all the signs and symptoms used to diagnose non severe

pneumonia, there is at least one of either lower chest wall indrawing, nasal flaring or

grunting. A diagnosis of very severe pneumonia is based on the presence of at least one of the

following: central cyanosis; inability to breastfeed/drink or vomiting; convulsions, lethargy

or unconsciousness; severe respiratory distress such as head nodding.41 The WHO severity

assessment does not include SpO2 measurement which is present in the BTS guidelines.

39

However, experts agree that blood oxygenation is an essential factor for evaluating CAP

severity and indeed constitutes the best indicator of the need for hospitalization.88

Treatment with antibiotics: Against the background of the reported causative role of viruses

in childhood pneumonia,30,45 it is appropriate not to treat every child with antibiotics.

However, making therapeutic decisions in the individual case may be difficult, because most

tests do not adequately differentiate viral from bacterial infections. Besides, some children

with severe pneumonia have mixed viral and bacterial agents.45 An additional treatment

challenge is the problem of bacterial resistance which has increased steadily over the years.40

The advent of bacterial resistance is related to the common practice of inappropriate

antibiotic usage in clinical conditions in which a viral aetiology is most likely, and/or the

illness is self limiting. The commonest clinical scenario which frequently attracts such an

inappropriate usage of antimicrobials is acute nasopharyngitis.

Table IV: Options of antibiotics in relation to age and clinical presentation of CAP.40

Age/ Clinical picture Inpatient Outpatient

Newborn

Ampicillin + gentamicin -

3 weeks to 3 months

interstitial infiltrate, not toxic

Macrolides Macrolides

4 months to 4 years Penicillin or ampicillin; add

macrolide if not responding.

Amoxicillin

5 years or older:

Alveolar infiltrate, pleural

effusion, toxic appearance

Penicillin or ampicillin; add

macrolide if not responding.

Macrolide; amoxicillin

5 years or older:

interstitial infiltrate

Macrolides; consider adding

a beta-lactam if not

responding.

Macrolides

Although none of the recent studies have addressed the issue of comparing the use of

antibiotics versus their non-use,40 it is logical to use them whenever a bacterial pneumonia is

the most probable diagnosis. Since an aetiologic diagnosis is more of the exception than the

rule in routine clinical practice, antibiotics are usually started on an empiric basis. The choice

40

of antibiotics in such situations is usually based on a summation of clinical features and the

regional prevalence data of CAP-causing pathogens in different age groups (Table IV).

General management: The general management of pneumonia for in-patients besides

oxygen therapy include adequate hydration (intravenous fluid as required), especially in

children whose intake has been significantly compromised by breathlessness and/or fatigue.39

Fluid intake should however be carefully monitored in such patients because pneumonia can

be complicated by SIADH.39 Furthermore, adequate nursing care via regular monitoring of

the vital signs, clearing the nostrils of mucus, provision of adequate calories via regular

feeding, as well as changing the position in bed for the child with impaired mental state are

all important general treatment measures required for a favorable disease outcome.

Oxygen therapy: Increased concentration of inspired oxygen is required when tissue

oxygenation is inadequate. Oxygen therapy not only improves the survival, but it may also

prevent substantial morbidity that may occur from prolonged hypoxemia in children who

survive.89 It may be a life-saving measure at the time it is required to treat the pneumonia.

The use of humidified oxygen is usually preferred, not only because it relieves hypoxaemia,

but also liquefies secretions and moistens the airway.39 The ultimate effect is a decrease in the

tenacity and viscosity of the usually copious respiratory secretions. The WHO recommends

administering oxygen, if there is ample supply, to children with signs and symptoms of

severe pneumonia and where supply is limited, to children with any of the following signs:

inability to feed and drink, cyanosis, respiratory rate greater than or equal to 70 breaths per

minute, or severe chest wall retractions.89 Oxygen is preferably administered at a flow rate of

0.5liter per minute for children younger than two months, and one liter per minute for older

children. However, if a pulse oximeter is available for monitoring the treatment of children

41

with severe pneumonia, the flow rate of the oxygen should be titrated against the SpO2 to

ensure adequate oxygenation of greater than 95%.89

Sources of oxygen may be from the oxygen cylinder or an oxygen concentrator.89 Oxygen

cylinders are heavy and difficult to transport, as they need to be transported to and fro for

refill, and to the point of use.89 Oxygen cylinders usually contain 100% oxygen. The other

major source of therapeutic oxygen is the oxygen concentrator. An oxygen concentrator

works by separating nitrogen from the oxygen in atmospheric air. Most of the available

oxygen concentrators use an electrically powered compressor to force compressed air through

synthetic aluminium silicate (zeolite) which reversibly binds nitrogen.89 This device usually

comes with an oxygen concentration indicator (OCI) which indicates the concentration of

oxygen being delivered at a time. The OCI consists of three lights; green when the oxygen

concentration being delivered is greater than 95%, orange when it is between 85-95% and red

if less than 85%.89 An oxygen concentrator delivers approximately 2-4l/min of gas,

containing over 90% oxygen.89 The concentration of the oxygen delivered is however less at

higher flow rates. Whereas oxygen concentrators are reliable, smaller, lighter and cheaper

than oxygen cylinders, a major limitation is that they are dependent on electricity, thus

restricting its usefulness in a country like Nigeria where power supply is neither reliable nor

dependable. It is also noteworthy that oxygen from both sources is completely dry, and would

need to be passed through a humidifier before delivery to the patient to achieve the required

humidified oxygen.

Oxygen can be delivered to the patient via one of the following devices which include face

masks, nasal prongs, nasal cannula, nasopharyngeal catheters, head box, or tents.89

42

JUSTIFICATION FOR THE STUDY

Pneumonia remains a major contributor to the high global, African regional and national

childhood mortality. In Nigeria, pneumonia accounts for an estimated 20-25% of childhood

deaths.59 Hypoxaemia remains a serious complication of severe respiratory illnesses in

general, and a strong risk factor of pneumonia-associated mortality in particular.8 10 80 In the

past, hypoxaemia has been overlooked in world-wide strategies for pneumonia control and

reducing child mortality. In most developing countries, including Nigeria where the majority

of pneumonia-related deaths occur, the situation is not different with respect to the paucity of

data on the role of hypoxaemia in pneumonia-related mortality.1 In developing countries, this

is due to the limited availability of the required tools (such as the pulse oximeter) for the early

detection and monitoring of hypoxaemia following oxygen therapy.7 Clearly, the identification

of a minimum set of clinical signs that can reliably detect the presence of hypoxaemia in

children with pneumonia will be an invaluable tool for the clinician in deciding when to

commence oxygen therapy. Furthermore, accurate identification of pneumonia-related

hypoxaemia in children will be crucial in determining the safety of continuing outpatient

treatment. In Nigeria and many other developing countries, the primary health care (PHC)

facility is usually the first point of contact for most children in the country requiring the

services of health care workers. These PHC facilities are usually manned by the lower cadres

of the health care team. Thus, the findings of the current study are likely to prove invaluable

for the health care workers at the primary health care centre especially in identifying the

criteria for referring patients to other facilities at the higher tiers of the health care system

where oxygen therapy is available.

To the best knowledge of the researcher, the aforementioned paucity of information on the

magnitude of pneumonia-related hypoxaemia is even more evident in Ilorin located in North

Central Nigeria where the current study was carried out. Also, there is the dearth of data on the

43

association between several risk factors of pneumonia and hypoxaemia. These knowledge

gaps are expected to be filled by the findings of the current study, which is also expected to

generate a data-base of the magnitude of pneumonia-associated hypoxaemia in Nigerian

children. In addition, by identifying the possible clinical signs that can detect hypoxaemia, the

current study also hopes to provide a data-base that can be incorporated into evolving national

guidelines on the management of children with pneumonia. Undoubtedly, such guidelines

would facilitate the early recognition of a child with hypoxaemia and thus, prompt referral

from PHC facilities to the higher tiers of the health system. It would also be a useful clinical

tool in the Paediatric Emergency Room, where oxygen use is currently being “rationed” due to

the limited availability. The clinical import of harnessing the use of the expected findings in

the in-patient care of children with CAP will be an ultimate reduction in the current

unacceptably high pneumonia-associated mortality in Nigeria, and the accomplishment of the

fourth MDG.

44

AIMS AND OBJECTIVES

A) General Objective:

To determine the clinical predictors of hypoxaemia in hospitalized children aged between

two months and up to five years with pneumonia at the University of Ilorin Teaching

Hospital (UITH), Ilorin, Kwara State.

B) Specific Objectives:

a) To determine the prevalence of hypoxaemia in children aged two months and up to five

years with pneumonia.

b) To identify the clinical predictors of hypoxaemia in children with pneumonia.

c) To determine the association between the risk factors of pneumonia and hypoxaemia.

d) To determine the relationship between various levels of hypoxaemia and the management

outcome of pneumonia.

45

MATERIALS AND METHOD

Study site

The study was conducted in the Emergency Paediatric Unit (EPU) and the Paediatric Medical

Ward of University of Ilorin Teaching Hospital (UITH). The hospital is located in Ilorin

South Local Government Area of Kwara State. Ilorin is the capital city of Kwara State,

situated in the North Central geopolitical zone of Nigeria. The hospital is a tertiary health

facility that serves as a referral centre, not only for patients from Kwara State, but also the

adjoining states of Osun, Niger, Kogi and Ekiti. It also provides significant primary and

secondary health care services to the general public. The EPU, which constituted the

principal recruitment site of the current study receive paediatric medical emergencies beyond

the neonatal period and up to the age of 14 years.

The yearly temperature in Ilorin ranges between 19.50 to 37.50C, while the ambient humidity

is usually between 42 and 45%.90 With a population of 777,667 and an annual growth rate of

2.3% (2006 census), Ilorin town is located at an altitude of 303m above sea level.90 Majority

of the inhabitants are predominantly artisans with poor income.

Study design

This was a descriptive cross-sectional study in which the subjects were children aged

between two months and up to five years diagnosed with pneumonia.

Sample size determination

The formula91 used for estimating the minimum sample size required for the study was:

n = z2pq

d2

Where:

n = the desired minimum sample size.

46

z = the standard normal deviation usually set at 1.96 which corresponds to 95% confidence

interval.

p = the proportion in the target population estimated to have a particular characteristic

(pneumonia). This was estimated at 11.1% from a previous study.4

q = the proportion in the target population who do not have a particular characteristic, i.e.

q = 1.0 – p = 1 – 0.111 = 0.889

d = tolerable margin of error, an observed difference of 5% or more taken as being

significant.

Therefore the minimum sample size required for the current study is:

n = (1.96)2×0.111 ×0.889

(0.05)2 = 151

However, for ease of statistical analysis, a total of 200 under-five children were recruited for

the study.

Subject recruitment

The subjects were children aged between two months and up to five years presenting at the

EPU of UITH with clinical features comprising cough of less than 28 days duration, fever,

difficult breathing, tachypnoea, and auscultatory findings of one or more of reduced breath

sound intensity, bronchial breath sounds, or crepitations.40

Subject recruitment was done at the initial presentation in EPU. All consecutive admissions

into the EPU with a diagnosis of pneumonia that fulfilled the inclusion criteria were enrolled.

Subjects were recruited by the researcher or, in the occasional case, by a trained paediatric

resident doctor. The study was completed within twelve months of commencement (June,

2011- May, 2012).

47

Inclusion criteria

Children aged between two months and up to five years admitted into the EPU with an

admission diagnosis of pneumonia based on the presence of cough of less than 28 days

duration, fever and two or more of the following clinical parameters of:

i. breathlessness,

ii. age-related tachypnoea (>50 breaths/minutes for infants aged two months up to one

year, and > 40 breaths/minute for children aged 12-59 months) .

iii. auscultatory findings of one or more of reduced breath sound intensity, bronchial

breath sounds and crepitations.40

Exclusion criteria

1) Children with severe anaemia defined as a haematocrit value of ≤15%.

2) Children with clinical features of shock like cold clammy extremities, weak thready

pulse and other parameters of poor peripheral perfusion.

3) Children that had previously been recruited for the study who re-present to the unit with

symptom recrudescence.

4) Children with sickle cell disease.

5) Children previously diagnosed to have bronchial asthma.

Ethical clearance

The study was approved by the Ethics and Research Committee of the University of Ilorin

Teaching Hospital (Appendix VI).

College approval

Approval was obtained from the National Postgraduate Medical College of Nigeria to

proceed with the study (Appendix VII).

48

Consent

The caregivers were interacted with and were provided with adequate explanations about the

study as contained in the information sheet (Appendix I). Subsequently, parental consent was

obtained by seeking their signatures or thumb printing on the form provided for that purpose

(Appendix II).

METHOD

On presentation at the EPU, each child had a full clinical evaluation after obtaining an

informed consent from the parent. A semi–structured questionnaire was administered to

obtain the clinical and socio-demographic data from each subject’s parent or guardian

(Appendix III).

Using the socio-economic classification scheme of Oyedeji (Appendix IV),92 the socio-

economic index score of each child was calculated based on the occupations and educational

attainments of their parents or caregiver. The mean of four scores (two for the father and two

for the mother) approximated to the nearest whole number was the social class assigned to

the child as proposed by the same author.92 For example, if the mother was a junior school

teacher (score = 3) and father a senior teacher (score=2) and the educational attainment of the

mother was primary six (score=4), and the father was a school certificate holder (score=2).

The socio-economic index score for this child was: (3+2+4+2)/4 =2.75, which approximated

to the nearest whole number was three.

The informant (mother/caregiver) was asked about their child's symptoms, specifically the

presence of symptoms such as cough, fever, inability to feed or drink, vomting, rapid or

difficult breathing, abnormal sleepiness and/or the child being difficult to wake or irritable.

The relevant parameters obtained from the physical examination included anthropometric

measurements (weight, height and mid- arm circumference in those aged one to five years).

The weight was measured using a bassinet weighing scale (Surgifriend Medicals, London,

49

England) in infants, and a beam balance weighing scale (Marsdens weighing machine,

London, England) in children who were able to stand unsupported. Both scales have a degree

of accuracy of 50g, and were calibrated prior to use. The standing height was measured to an

accuracy of 0.1cm using a stadiometer. The mid-arm circumference (MAC) was measured to

the nearest 0.1cm using a non-flexible tape measure. The MAC was taken at the point mid-

way between the olecranon process of the ulna and the acromion process of the scapula.

The presence or absence of the relevant clinical signs like tachypnoea, nasal flaring, wheeze,

central cyanosis and chest indrawing were also noted. The respiratory rate was counted by

visual inspection of upward movement of the abdominal and/or chest wall while the child

was calm for one minute. The presence/absence of fast breathing in the individual subject

was determined using the age-related cut-off values of >50 breaths/minute for infants aged

two months up to one year, and >40 breaths/minute for children aged 12-59months. To

determine the presence of chest indrawing the child’s clothing were removed gently to enable

visualization of the lower chest wall. Chest wall indrawing was identified as inward

movement of the lower chest wall on breathing in, with the child lying flat on either the

mother's lap, or the examination couch. If the child was not quiet, examination was delayed

until the mother was able to make the child calm enough. Central cyanosis was determined by

bluish discoloration of the tongue and/or buccal mucosa. Percussion was done over the inter-

costal spaces (anterior and posterior), and the presence of resonant, dull or hyper-resonant

percussion notes were noted. Similarly, auscultatory signs like reduction in the intensity of

breath sounds, presence of crepitations, rhonchi, bronchial or transmitted sounds were

recorded in the study proforma. The clinical findings/observations made were recorded by the

investigator, and/or a trained assistant whose expertise regarding study guidelines had been

verified by the investigator as well as her supervisors.

50

Haemoglobin oxygen saturation (SpO2) was measured by attaching a Smartsigns® Liteplus

CE 0088 pulse oximeter (Huntleigh Healthcare, Cardiff, United Kingdom) to a finger using

an appropriately sized paediatric sensor. This was done as soon as possible after presentation

before oxygen administration as required. The oxygen saturation was recorded after a stable

reading was obtained for at least one minute while the child was breathing room air. The

oxygen saturation level of the researcher obtaining the measurement was recorded at the

beginning of each day of data collection. This was to serve as a control and confirm that the

oximeter was functioning appropriately. For the purpose of the current study, hypoxaemia

was defined as an arterial oxygen saturation of less than 90% as recorded by pulse oximetry.

8,32 Also, in the present study, the various levels of SpO2 were divided as ‘‘greater than 95%,

93-95%, 90-92%, 86-89%, and less than or equal to 85%’’.

The severity of pneumonia in each subject was graded (mild, moderate, severe) using the

British Thoracic Society (BTS) guidelines on the management of CAP in children.88 The

presence of two or more features in each category was used to grade the severity of

pneumonia in the subjects (Appendix V). Subjects with complications of pneumonia at

presentation were considered as having severe pneumonia.88

Chest radiographs were obtained in all subjects within 24 hours of presentation. Radiographic

features were recorded as either normal, presence of patchy opacities in one or more lobes, or

lobar/segmental consolidation with or without an air bronchogram. Also, the presence of

radiographic features of effusion, or other intra-thoracic complications such as pneumothorax

were identified and recorded. In order to validate the above radiographic findings, the

radiograph findings were corroborated by a Consultant Radiologist. Using a combination of

clinical and radiographic parameters, subjects were grouped as having either lobar or

bronchopneumonia.

51

All subjects had a blood specimen obtained for bacterial culture to determine the possible

causative agent, and haematologic parameters like packed cell volume (PCV), total and

differential white blood cell (WBC) count. All subjects were treated with the most

appropriate medications according to the current institutional guidelines. Furthermore, the

patient’s management was in no way hindered by his or her recruitment into the current

study.

Blood sample collection

Using strict aseptic techniques, the selected body site for blood sample collection was wiped

thoroughly by the investigator, or in the occasional case a trained paediatric resident, using

cotton wool soaked in 70% alcohol and chlorhexidine. Sufficient time was allowed for the

skin of the selected site to dry prior to the venepuncture.93 A fixed hypodermic needle was

used to collect four millilitres of whole blood from an accessible peripheral vein into a five

ml syringe. A separate needle was attached to the syringe for inoculating two millilitres of the

venous blood into the bottle containing the blood culture media. This was done by puncturing

the sealed opening at the top after wiping with wet cotton wool (soaked in 70% alchohol and

clorhexidine). The remaining two millilitres were transferred into a sample bottle containing

ethylene-diamine-tetra-acetate (EDTA), and gently mixed to prevent clotting. This latter

sample was used for obtaining the relevant haematological indices like total and differential

WBC counts. For the purpose of determining the haematocrit, heparinised capillary tube

sample was taken at an angle of 450 from the blood surface and the tube subsequently sealed

with plasticine at one end before centrifugation.

Laboratory Techniques

Blood culture bottles were incubated at 370C and examined for evidence of growth (turbidity,

cotton balls, bubbles, clots) on a daily basis by the microbiologist(s) in the laboratory.93

Subsequently, films were made from individual colonies when growths were observed. A

52

Gram stain examination was carried out on each sample. Whenever evidence of growth was

noticed, subculturing was done on MacConkey, chocolate and sheep blood agar. The blood

culture findings were corroborated by a Consultant Microbiologist. Inoculated media was

discarded on the seventh day whenever there was no evidence of growth.

The packed cell volume (pcv) was determined by spinning the capillary tube containing

blood samples in a micro-centrifuge at a centrifugal force of c12, 000g for five minutes by

the investigator. In the occasional case, this was determined by the trained paediatric resident

doctor. Subsequently, the reading was done using a haematocrit reader. The WBC and

differential count was done with an automated blood analyzer Symex KX 21® (Sysmex

Corporation, Kobe, Japan) by the senior laboratory scientist(s) and the results were recorded

in the study proforma.

53

Data analysis

Data was analyzed using the IBM® SPSS version 20.0 (IBM corporation, Virginia, U.S.A.)

2011 for windows software package. The data collected on the proforma were transferred into

a master sheet using numerical codes. A nutritional anthropometry program, NutriStat® of

Epi-info version 3.5.1(2008) was used to determine the percentage and z-score for age of

each child based on the WHO Growth Reference dataset.94

After the generation of frequency tables and simple proportions, the chi-square (χ2) and

Student’s t-tests were used to identify significant differences for categorical and continuous

variables respectively. Analysis of variance (ANOVA) test was used in comparing the means

when there were more than two groups for comparison. The distributions of discrete clinical

signs between hypoxaemic and non-hypoxaemic children were compared by using the χ2 test.

The Yates corrected value or the Fisher's exact test was used for testing the significance of

associations between cells with small numbers (<5) as appropriate. The sensitivity,

specificity, as well as positive and negative predictive values (PPV and NPV respectively)

was determined for the symptoms and signs in predicting the presence of hypoxaemia. Also,

a linear regression analysis was done to determine the best independent combinations of

symptoms and clinical signs for predicting hypoxaemia. In determining the correlation

between some risk factors of pneumonia and the SpO2 levels, the Spearman’s rank

correlation was used for categorical variables while the Pearsons correlation test was used

for quantitative variables. A p-value of <0.05 was considered significant.

54

RESULTS

Age and gender distribution of the children with pneumonia

A total of 200 children with pneumonia were recruited into the study. One hundred and

thirteen (56.5%) of the children were infants as shown in Table V. The mean(SD) age was

14.3 (13.5) months while the male: female (M:F) ratio was 1.5:1.

Table V: Age and gender distribution of the children with pneumonia

Age group

(months)

Male

n(%)

Female

n(%)

Total

n(%)

2-<12 64(32.0) 49(24.5) 113(56.5)

12-<24 32(16.0) 14(7.0) 46(23.0)

24-<36 16(8.0) 10(5.0) 26(13.0)

36-<48 1(0.5) 3(1.5) 4(2.0)

48-<60 6(3.0) 5(2.5) 11(5.5)

Total 119(59.5) 81(40.5) 200(100.0)

55

Some risk factors of pneumonia in the study population

Thirteen (6.5%) of the children with pneumonia had never received any vaccination, while

187 (93.5%) had received at least one or more types of vaccination. Seventeen (8.5%) of the

children had concomitant measles infection, five (2.5%) had HIV co-infection while three

(1.5%) had pertussis as a co-morbid illness with the pneumonia. The distribution of some of

the other risk factors of pneumonia among the study population is shown in Table VI.

Table VI: Some risk factors of pneumonia in the study population

Parameter Frequency Percentage Cumulative percent

Family type

Monogamous 169 84.5 84.5

Polygamous 31 15.5 100.0

Number of siblings

≤3 126 63.0 63.0

>3 31 15.5 78.5

None 43 21.5 100.0

Birth interval

None 43 21.5 21.5

<24months 33 16.5 38.0

≥24months 124 62.0 100.0

Smoking in the house

Yes 19 9.5 9.5

No 181 90.5 100.0

Attendance at day care

centre

Yes 25 12.5 12.5

No 175 87.5 100.0

Indoor cooking

Yes 153 76.5 76.5

No 47 34.5 100.0

Cooking with firewood

Yes 21 10.5 10.5

No 179 89.5 100.0

Exclusive breastfeeding

Yes 160 80 80.0

No 40 20 100.0

56

Clinical features in the study population

All the children presented with cough and fever as shown in Figure 5. Other common

respiratory symptoms were difficult breathing (91.0%), nasal discharge (43.5%) and fast

breathing (38.5%). The most common non-respiratory symptoms were inability to feed

(25.5%) and vomiting (24.0%).

Figure 5: Symptoms of pneumonia in the study population

200(100.0%)

200(100.0%)

182(91.0%)

87(43.5%)

77(38.5%)

51(25.5%)

48(24.0%)

39(19.5%)

35(17.5%)

29(14.5%)

23(11.5%)

21(10.5%)

16(8.0%)

6(3.0%)

4(2.0%)

0 50 100 150 200 250

fever

cough

difficult breathing

nasal discharge

fast breathing

inability to feed

vomiting

inability to drink

lethargy

restlessness

skin rash

noisy breathing

diarrhoea

convulsion

loss of consciousness

frequency

sym

pto

ms

frequency

57

Age-related tachypnoea, nasal flaring, reduced intensity of breath sounds and crepitations

were the most common findings and were identified in 191 (95.5%), 181 (90.5%), 176

(88.0%) and 162 (81.0%) subjects respectively. Central cyanosis and head nodding were the

least common findings identified in six (3.0%) and four (2.0%) of the subjects respectively.

The other physical findings in the study population with their frequency of occurrence are

shown in Table VII.

Table VII: The physical examination findings in children with pneumonia

Examination findings Frequency Percentage

Age-related tachypnoea 191 95.5

Nasal flaring 181 90.5

Diminished breath sounds 176 88.0

Crepitations 162 81.0

Febrile≥37.5oC 145 72.5

Lower chest wall indrawing 127 63.5

Hepatomegaly 127 63.5

Intercostal recession 91 45.5

Pallor 64 32.0

Tender hepatomegaly 61 30.5

Grunting 59 29.5

Rhinorrhoea 53 26.6

Dehydration 50 25.0

Abnormal percussion findings 46 23.0

Splenomegaly 22 11.0

Snuffle 21 10.5

Bronchial breath sounds 19 9.5

Unconsciousness 8 4.0

Central cyanosis 6 3.0

Head nodding 4 2.0

58

Anthropometry of the study population

As shown in Table VIII, the mean(SD) weight of the children recruited was 7.8(3.1) kg,

while the mean(SD) height was 71.2(31.5) cm. Ninety (45.0%) of the children had a weight

for age percentage which was estimated as less than 80% of the expected while 18 (20.5%) of

the 87 children aged between one and five years had a mid- arm circumference less than 13.5

cm.

Table VIII: Anthropometric measurements in children with pneumonia

Anthropometry Frequency Percentage Range Mean±SD

Weight (Kg) 200 100.0 3.0-20.0 7.8±3.1

Height (cm) 200 100.0 50.0-114.5 71.2±31.5

Weight for age percentage (%)

≤80 90 45.0 43.4-79.9 69.8±8.2

>80 110 55.0 80.6-140.6 99.4±11.5

Total 200

100.0 43.4 – 140.6 83.3±15.9

Height for age percentage (%)

≤95 101 50.5 75.3-94.9 89.7±4.4

>95 99 49.5 95.1-128.3 101.5±6.1

Total 200

100.0 75.3 – 128.3 95.6±7.9

Weight for height percentage (%)

≤90 90 45.0 38.9-88.9 77.4±10.6

>90 110 55.0 90.4-175.6 108.2±16.7

Total 200

100.0 38.9- 175.6 94.3±21.0

Weight for age z-score

<-1 125 62.5 -5.7- -1.1 -2.3±0.9

≥-1 75 37.5 -1.0- 3.2 -0.1±0.8

Total 200

100.0 -5.7- 3.2 -1.5±1.4

Height for age z-score

<-1 109 54.5 -6.3 - -1.1 -2.5±1.2

≥-1 91 45.5 -1 – 7.0 0.5±1.5

Total 200

100.0 -6.3- 7.0 -1.1±2.0

Weight for height z-score

<-1 93 46.5 -7.8- 1.1 -2.5±1.3

≥-1 107 53.5 -1.0- 5.6 0.7±1.4

Total 200

100.0 -7.8- 5.6 -0.8±2.1

Mid- arm circumference (cm)

<13.5 18 20.5 10.0-13.0 12.5±0.8

≥13.5 69 79.5 13.5-18.0 14.8±0.9

Total 87 100.0 10.0-18.0 14.3±1.3

59

Distribution of pneumonia among the study population

Bronchopneumonia accounted for the diagnosis in 168(84.0%) of the children while lobar

pneumonia was diagnosed in 32(16.0%) of the children recruited. Twelve (6.0%) of the

children were classified with moderate pneumonia while 188(94.0%) had severe pneumonia.

Bacteria isolates in the children with pneumonia

A positive growth was identified on blood culture in 67(33.5%) children, while the pleural

aspirate yielded a positive growth in three (20.0%) children. Staphylococcus aureus was the

most common bacterial agent present accounting for 21 (31.3%) of the 67 positive blood

culture and two (66.7%) of the three positive pleural aspirate cultures as shown in Table IX

Table IX: Bacterial agents of pneumonia in the subjects

Culture Findings Frequency Percentage

Blood culture growth

Present 67 33.5

Absent 133 66.5

Total 200 100.0

Type of organism in blood culture

Staphylococcus aureus 21 31.3

Klebsiella spp. 13 19.4

Mixed growth 9 13.4

Coagulase negative Staphylococcus 9 13.4

Escherichia coli 4 6.0

Coliforms 3 4.5

Micrococcus spp. 2 3.0

Streptococcus pyogenes 2 3.0

Non-haemolytic Streptococci 1 1.5

Actinobacter spp. 1 1.5

Pseudomonas spp. 1 1.5

Streptococcus pneumoniae 1 1.5

Total 67 100.0

Pleural aspirate growth Present 3 20.0

Absent 12 80.0

Total 15 100

Type of organism in pleural fluid Staphylococcus aureus 2 66.7

Streptococcus pyogenes 1 33.3

Total 3 100.0

60

Hypoxaemia in the study population

The mean(SD) SpO2 level of the 200 children recruited was 90.4(8.9) % with a range of 47-

100%. Using SpO2 level of less than 90% as the cut-off, the prevalence of hypoxaemia in the

children with pneumonia was 41.5% and the mean(SD) SpO2 was 82.3(8.1) % as shown in

Table X.

Table X: Hypoxaemia and SpO2 levels in children with pneumonia

Parameter Frequency Percentage Mean±SD (%)

Hypoxaemia

Yes 83 41.5 82.3±8.1

No 117 58.5 96.2±2.8

Total 200 100.0 90.4±8.9

Levels of SpO2 (%)

>95 75 37.5 98.0±1.5

93-95 24 12.0 93.8±0.9

90-92 18 9.0 91.8±0.4

86-89 34 17.0 88.1±1.0

≤85 49 24.5 78.2±8.5

61

Table XI shows that 83 (44.1%) children with severe pneumonia had hypoxaemia and this

proportion was significantly higher compared to none recorded among those with moderate

pneumonia (p=0.003). Furthermore, 62.5% of the children with lobar pneumonia had

hypoxaemia which was significantly higher than the corresponding value of 37.5% recorded

in those with bronchopneumonia (p =0.009).

Table XI: Hypoxaemia based on the severity and type of pneumonia

Pneumonia Hypoxaemia present Total χ2 p-value

Yes No

Severity

Moderate 0(0.0) 12(100.0) 12 # 0.003

Severe 83(44.1) 105(55.9) 188

Type

Bronchopneumonia 63(37.5) 105(62.5) 168 6.920 0.009

Lobar pneumonia 20(62.5) 12(37.5) 32

# = Fisher’s exact test

62

Clinical predictors (symptoms) of hypoxaemia among children with pneumonia

As shown in Table XII, poor drinking, restlessness, lethargy and difficult breathing were

identified as the significant symptoms that predicted the presence of hypoxaemia in the

subjects (p<0.05 each). Difficult breathing had the highest sensitivity (98.8%) but a low

specificity of 14.1% while the PPV was 45.1%. Restlessness had the highest specificity of

91.5%, a moderate PPV of 65.5% but a low sensitivity of 22.9%.

Table XII: Pneumonia symptoms as predictors of hypoxaemia in the subjects

Symptoms

Hypoxaemia p-value* Sensitivity

(%)

Specificity

(%)

PPV

(%)

NPV

(%) Yes No

Inability to feed

Yes 27 24 0.055 32.5 79.5 52.9 62.4

No 56 93

Poor drinking

Yes 23 16 0.014 27.7 86.3 59.0 62.7

No 60 101

Restlessness

Yes 19 10 0.005 22.9 91.5 65.5 62.6

No 64 107

Lethargy

Yes 34 28 0.010 41.0 76.1 54.8 64.5

No 49 89

Nasal discharge

Yes 30 57 0.077 36.1 51.3 34.5 53.1

No 53 60

Difficult breathing

Yes 82 100 0.001 98.8 14.5 45.1 94.4

No 1 17

Fast breathing

Yes 31 46 0.447 37.3 60.7 40.3 57.7

No 52 71

Noisy breathing

Yes 11 10 0.285 13.3 91.5 52.4 59.8

No 72 107

* = chi-square test derived; PPV=positive predictive value; NPV=negative predictive value

63

Clinical predictors (examination findings) of hypoxaemia among children with

pneumonia

As shown in Tables XIIIA and XIIIB, clinical features that attained statistical significance

(p=<0.05) amongst the children with hypoxaemia on examination were pallor, dehydration

(moderate and severe), central cyanosis, grunting, intercostal recession and lower chest

indrawing. Other significant findings on clinical examination were the presence of abnormal

percussion notes, bronchial breath sounds and tender hepatomegaly (each p=<0.05).

The presence of intercostal recessions had the highest sensitivity of 100% while central

cyanosis had the highest specificity and PPV of 100% each.

Table XIIIA: Clinical parameters as predictors of hypoxaemia in the children with

pneumonia-I Clinical feature

(Examination I)

Hypoxaemia p-value Sensitivity

(%)

Specificity

(%)

PPV

(%)

NPV

(%) Yes No

Febrile ≥37.5oC

Yes 61 84 0.791* 73.5 28.2 42.1 60.0

No 22 33

Pallor

Yes 38 26 0.001* 45.8 77.8 59.4 66.9

No 45 91

Moderate/severe

dehydration

Yes 13 7 0.025* 15.7 94.0 65.0 61.1

No 70 110

Tachypnoea

Yes 77 114 0.112# 92.8 2.6 40.3 33.3

No 6 3

Central cyanosis

Yes 6 0 0.005# 7.2 100.0 100.0 60.3

No 77 117

Grunting

Yes 37 22 0.001* 44.6 81.2 62.7 67.4

No 46 95

Rhinorrhoea

Yes 17 37 0.097* 20.5 69.0 32.1 54.8

No 66 80

* = chi-square test derived; # = Fisher’s exact test derived; PPV=positive predictive value;

NPV=negative predictive value

64

Table XIIIB: Clinical parameters as predictors of hypoxaemia in the children with

pneumonia-II

Clinical feature

(Examination )

Hypoxaemia p-

value

Sensitivity

(%)

Specificity

(%)

PPV

(%)

NPV

(%) Yes No

Nasal flaring

Yes 79 102 0.057* 95.8 12.8 43.6 78.9

No 4 15

Intercostal recession

Yes 83 99 0.001* 100.0 15.4 45.6 100.0

No 0 18

Lower chest indrawing

Yes 72 55 0.001* 86.7 53.3 56.7 84.9

No 11 62

Head nodding

Yes 3 1 0.195# 3.6 99.1 75.0 59.2

No 80 116

Abnormal percussion note

Yes 31 15 0.001* 37.3 87.2 67.4 66.2

No 52 102

Reduced BS intensity

Yes 77 98 0.058* 92..8 16.2 44.0 75.0

No 6 19

Crepitations

Yes 71 91 0.168* 85.5 22.2 43.8 68.4

No 12 26

Bronchial BS

Yes 14 5 0.003* 16.9 95.7 73.7 61.9

No 69 112

Tender hepatomegaly

Yes 40 21 0.001* 48.2 82.1 65.6 69.1

No 43 96

Splenomegaly

Yes 6 16 0.151* 7.2 86.3 27.3 56.7

No 77 101

Unconsciousness

Yes 6 2 0.056# 7.2 98.3 75.0 59.9

No 77 115

* = chi-square test derived; # = Fisher’s exact test derived; PPV=positive predictive value;

NPV=negative predictive value; BS= breath sounds

65

In order to exclude the effect of confounding variables in predicting hypoxaemia among the

children with pneumonia, a subsequent linear regression analysis of the relative contribution

of these variables was carried out list-wise. Table XIV shows that the clinical features that

remained significant were restlessness, lower chest wall indrawing, bronchial breath sounds

and tender hepatomegaly (p<0.05 each). The model shows that the effect of clinical features

on the presence of hypoxaemia is 44.8%. The goodness-of-fit model gave an F-value of

16.851; df=4, p =0.001.

Table XIV: Linear regression model of the clinical features and the presence of

hypoxaemia in children with pneumonia

Clinical feature Beta Co-efficient t p-value

Inability to feed 0.009 0.101 0.920

Inability to drink 0.062 0.679 0.499

Restlessness 0.181 2.165 0.033

Vomiting 0.007 0.083 0.934

Diarrhoea -0.011 -0.129 0.897

Convulsion -0.125 -1.480 0.143

Nasal discharge 0.059 0.709 0.480

Difficult breathing 0.053 0.615 0.540

Fast breathing 0.064 0.769 0.444

Noisy breathing -0.054 -0.632 0.529

Dehydration 0.092 1.047 0.298

Febrile ≥37.5 0.004 0.048 0.962

Age-related tachypnoea -0.057 -0.685 0.496

Pallor 0.113 1.137 0.259

Central cyanosis 0.102 1.194 0.236

Grunting 0.025 0.262 0.794

Snuffles -0.056 -0.675 0.502

Rhinorrhoea -0.045 -0.546 0.586

Nasal flaring -0.030 -0.350 0.727

Intercostal recession 0.012 0.132 0.895

Lower chest indrawing 0.354 4.250 0.001

Head nodding 0.002 0.020 0.984

Abnormal percussion notes 0.075 0.704 0.483

Abnormal breath sound intensity -0.024 -0.280 0.780

Crepitations 0.039 0.466 0.642

Bronchial breath sound 0.271 3.168 0.002

Hepatomegaly 0.165 1.841 0.069

Tender hepatomegaly 0.284 3.253 0.002

Splenomegaly -0.041 -0.482 0.631

Unconscious state -0.116 -1.410 0.162

66

Relationship between risk factors of pneumonia and the presence of hypoxaemia

Table XVA shows that 59(49.2%) of the children in the low social class had hypoxaemia

which was significantly higher when compared with 24(30.0%) of the children from a high

social class (p=0.007). Also, a significantly higher proportion of children with a high birth

order had hypoxaemia compared with the corresponding proportion in those with a lower

birth order, p=0.026. Furthermore, hypoxaemia was significantly higher in children of

mothers who had primary school education compared with the corresponding proportion of

children whose mothers had at least secondary school education, p=0.022 (Table XVIA).

Table XVA: Hypoxaemia and risk factors of pneumonia in the study population-Group 1

Risk factors 1 Hypoxaemia p-value*

n Yes (%) No (%)

Age group (months)

2-<12 113 52(46.0) 61(54.0) 0.140

12-<60 87 31(35.6) 56(64.4)

Gender

Male 119 51(42.9) 68(57.1) 0.637

Female 81 32(39.5) 49(60.5)

Social class of child

High(I,II) 80 24(30.0) 56(70.0) 0.007

Low(III,IV,V) 120 59(49.2) 61(50.8)

Maternal educational level

≥Secondary 106 36(34.0) 70(66.0) 0.022

≤Primary 94 47(50.0) 47(50.0)

Maternal age group (years)

<35 158 61(38.6) 97(61.4) 0.107

≥35 44 22(52.4) 20(47.6)

Family type

Monogamous 168 69(41.3) 99(58.7) 0.778

Polygamous 32 14(45.2) 18(54.8)

Number of siblings

≤3 169 68(40.2) 101(59.8) 0.397

>3 31 15(48.4) 16(51.6)

Birth order

1st - 4th child 174 67(38.5) 107(61.5) 0.026

≥ 5th child 26 16(61.5) 10(38.5)

Exclusive breastfeeding

Yes 160 66(41.3) 94(57.9) 0.886

No 40 17(42.5) 23(57.5)

*= chi-square test derived

67

Also, Table XVB shows that hypoxaemia was significantly higher among the unvaccinated

children compared to those who were vaccinated, p<0.036.

Table XVB: Hypoxaemia and risk factors of pneumonia in the study population (Group

2)

Risk factor 2 Hypoxaemia p-value*

n Yes (%) No (%)

Smoking in the house

Yes 19 11(57.9) 8(42.1) 0.127

No 181 72(39.8) 109(60.2)

Indoor cooking

Yes 153 62(40.5) 91(59.5) 0.613

No 47 21(44.7) 26(55.3)

Cooking with firewood

Yes 21 11(52.4) 10(47.6) 0.285

No 179 72(40.2) 107(59.8)

Attendance at day-care

Yes 25 9(36.0) 16(64.0) 0.551

No 175 74(42.3) 101(57.7)

Immunization

None 13 9(69.2) 4(30.8) 0.036

Yes 187 74(39.6) 113(60.4)

Pertussis

Present 3 1(33.3) 2(66.7) 0.999#

Absent 197 82(41.6) 115(58.4)

Intercurrent Measles

Present 17 9(52.9) 8(47.1) 0.319

Absent 183 74(40.4) 109(59.6)

Positive blood culture

Present 67 33(49.3) 34(50.7) 0.140

Absent 133 51(38.3) 82(61.7)

*=chi-square test derived; # =Fisher’s Exact test derived.

68

Correlation of the risk factors of pneumonia and the presence of hypoxaemia

As shown in Table XVI, the social class of the child was identified to have a negative

correlation with the presence of hpoxaemia. Also, factors such as the maternal age, maternal

literacy level, the birth order of the child and absence of immunization had a negative

correlation with the presence of hypoxaemia.

Table XVI: Correlation of the risk factors of pneumonia with the presence of

hypoxaemia

Risk Factor Correlation (r) p-value

Age (months) 0.087 0.221

Social class -0.191 0.007

Maternal age (years) -0.151 0.032

Maternal literacy -0.162 0.022

Family type 0.013 0.853

Birth order -0.154 0.030

Sibling group 0.064 0.365

Birth interval -0.022 0.753

Smoking in the house 0.108 0.129

Attendance at daycare -0.042 0.553

Immunization status -0.148 0.036

Pertussis -0.020 0.774

Measles 0.071 0.319

Exclusive breastfeeding -0.010 0.887

Duration of exclusive breastfeeding -0.063 0.378

Indoor cooking -0.036 0.615

Cooking with firewood 0.076 0.287

WAP 0.095 0.182

HAP 0.063 0.378

WHP 0.013 0.852

WAZ 0.107 0.130

WHZ -0.012 0.865

HAZ 0.016 0.827

WAP (weight for age percentage), HAP (height for age percentage), WHP (weight for height

percentage), WHZ (weight for height –z-score), WAZ (weight for age-z-score) and HAZ

(height for age-z-score)

69

Distribution of complications in children with pneumonia

A total of 93 complications were recorded in 73(36.5%) of the 200 children with pneumonia;

52 (27.5%) had one complication while 21(10.5%) children had more than one complication.

As shown in Figure 6, heart failure was the single most common complication recorded in the

children with pneumonia.

Figure 6: Complications of pneumonia in the study population

44(47.3%)

10(10.8%)

0 0 0 0

1(1.1%)

0 0

17(18.3%)

7(7.5%)

4(4.2%) 3

(3.1%) 2(2.2%)

2(2.2%) (1.1%)

11

(1.1%)1

(1.1%)

freq

uen

cy o

f co

mp

licati

on

type of complication

singly

combination

70

Hypoxaemia and complications in children with pneumonia

Table XVII shows that a significantly higher proportion of the subjects with pneumonia-

associated complications had hypoxaemia compared with the corresponding proportion in

those without hypoxaemia, p=0.001.

Table XVII shows that SpO2 levels of ≤ 85% was associated with a significantly higher

proportion of children with complications when compared with those with SpO2 of >95%.

Table XVII: Pneumonia-associated complications and hypoxaemia in the subjects

Parameter Complication χ2 p-value

Present Absent

Hypoxaemia

Present 48(57.8) 35(42.2) 27.854 0.001

Absent 25(21.4) 92(78.6)

Levels of SpO2 (%)

>95 10(13.3) 65(86.7) 35.303 0.001

93-95 7(29.2) 17(70.8)

90-92 8(44.4) 10(55.6)

86-89 18(52.9) 16(47.1)

≤85 30 (61.8) 19(38.2)

Severity of pneumonia

Moderate 0(0.0) 12(100.0) # 0.007

Severe 73(38.8) 115(61.2)

Type of pneumonia

Bronchopneumonia 51(29.8) 117(70.2) 17.734 0.001

Lobar pneumonia 22(68.8) 10(31.2)

Admission outcome

Survived 56(30.6) 127(69.4) 32.323 0.001

Died 17(100.0) 0(0.0)

# =Fisher’s Exact test derived

71

Treatment outcome in the children with pneumonia

Seventeen of the children with pneumonia died giving a case fatality of 8.5%. Ten (58.8%) of

those who died were aged less than 12months, while the remaining seven (41.2%) were aged

between 12 and 60months. Furthermore, six (18.7%) of the 32 children with lobar pneumonia

died, while 11(6.5%) of the 168 children with bronchopneumonia had a fatal outcome.

All the children who died had hypoxaemia while no fatality was recorded in the children

without hypoxaemia, and this difference in the treatment outcome was significant (p=0.001).

(Table XVIII).

Table XVIII: Hypoxaemia and treatment outcome in the children with pneumonia

Parameter Outcome of treatment p-value*

Survived

n (%)

Died

n (%)

Hypoxaemia

Present 66(79.5) 17(20.5) 0.001

Absent 117(100.0) 0(0.0)

Levels of SpO2 (%)

>95 75(100.0) 0(0.0)

93-95 24(100.0) 0(0.0)

90-92 18(100.0) 0(0.0)

86-89 28(81.8) 6(18.2) 0.673a

≤85 38(78.0) 11(22.0)

*= chi-square test derived

a: compares outcome among those with levels of SpO2 ‘86-89%’ and ‘≤85’

72

The mean SpO2 level in children with hypoxaemia was significantly lower than the recorded

value in those without hypoxaemia, p=0.001. Furthermore, the mean SpO2 level of 78.3% in

the fatal cases was significantly lower than the corresponding value of 91.5% recorded in the

survivors, p=0.001. The relationship between the recorded pulse oximeter values and some

other parameters are shown in Table XIX.

Table XIX: The pulse oximeter readings and outcome in children with pneumonia

Parameter n(%) Pulse oximeter reading (%) t p-value

Range Mean±SD

Hypoxaemia

Present 83(41.5) 47-89 82.3±8.1 -17.118 0.001

Absent 117(58.5) 91-100 96.2±2.8

Levels of SpO2 (%)

>95 75(37.5) 96-100 98.0±1.5a 161.403* 0.001

93-95 24(12.0) 93-95 93.8±0.9b

90-92 18(9.0) 91-92 91.8±0.4c

86-89 34(17.0) 86-89 88.1±1.0c

≤85 49(24.5) 47-85 78.2±8.5d

Admission outcome

Survived 183(91.5) 55-100 91.5±7.8 6.437 0.001

Died 17(8.5) 47-89 78.3±10.9

Type of pneumonia

Bronchopneumonia 168(84.0) 47-100 91.0±9.0 2.029 0.044

Lobar pneumonia 32(16.0) 64-99 87.5±7.9

Severity of pneumonia

Moderate 12(6.0) 94-100 97.1±2.2 2.729 0.007

Severe 188(94.0) 47-100 90.0±9.0

Complication

Present 73(36.5) 47-100 85.6±10.0 -6.392 0.001

Absent 127(63.5) 55-100 93.2±6.8

Number of complication

None 127(63.5) 55-100 93.2±6.8a 21.615* 0.001

One 52(26.0) 60-100 86.4±9.1b

>One 21(10.5) 47-99 83.4±12.0b

*= F-value (derived from ANOVA) a, b,c, d: Duncan multiple range test shows that means with the same letter are not statistically

different at p<0.05.

73

The relationship between duration of hospitalization and the presence of hypoxaemia in

children with pneumonia

The mean (SD) duration of hospital admission among the subjects with pneumonia was 5.7

(4.7) days. Table XX shows that the mean (SD) duration of hospital stay of 6.9(6.4) days in

subjects with hypoxaemia was significantly longer than the corresponding value of 4.9(2.7)

days recorded in those without hypoxaemia (p=0.002). Also, the mean duration of

hospitalization increased as the SpO2 levels reduced, and this observation was significant at

p=0.002. Furthermore, the mean duration of hospital stay in children with lobar pneumonia

was significantly longer than the corresponding value recorded in those with

bronchopneumonia, p=0.001.(Table XX)

Subjects with pneumonia-associated complications had a significantly longer mean duration

of hospitalization compared with the corresponding value in subjects without complications,

p=0.001. Also, Table XX shows that the mean duration of hospitalization was significantly

longer in children with two or more pneumonia-associated complications compared with the

corresponding value in those who had either one pneumonia complication or none (p=0.001).

74

Table XX: The duration of hospitalization and hypoxaemia in the children with

pneumonia

Parameter n(%) Duration of hospitalization (days) t p-value

Range Mean±SD

Hypoxaemia

Present 83(41.5) 0.2-33 6.9±6.4 3.131 0.002

Absent 117(58.5) 1-19 4.9±2.7

Levels of SpO2 (%)

>95 75(37.5) 1-10 4.2±2.0a 4.296* 0.002

93-95 24(12.0) 1-13 5.4±2.7a

90-92 18(9.0) 3-19 6.7±4.2ab

86-89 34(17.0) 0.3-32 7.9±7.0b

≤85 49(24.5) 0.2-33 6.3±6.0ab

Admission outcome

Survived 183(91.5) 1-33 6.1±4.7 3.560 0.001

Died 17(8.5) 0-12 1.9±3.0

Type of pneumonia

Bronchopneumonia 168(84.0) 0.2-33 5.1±3.8 -1.812 0.001

Lobar pneumonia 32(16.0) 0.3-32 9.0±7.2

Severity of pneumonia

Moderate 12(6.0) 2-9 3.3±2.1 -1.812 0.072

Severe 188(94.0) 0.3-33 5.9±4.8

Complication

Present 73(36.5) 0.2-33 7.4±6.7 3.859 0.001

Absent 127(63.5) 1-22 4.8±2.7

Number of complication

None 127(63.5) 1-22 4.8±2.7a 13.316* 0.001

One 52(26.0) 0-32 6.3±5.5a

>One 21(10.5) 0-33 10.1±8.4b

*= F-value (derived from ANOVA) a, b: Duncan multiple range test shows that means with the same letter are not statistically

different at p<0.05.

75

The relationship between the duration of oxygen therapy and presence of hypoxaemia

in the study population

The mean (SD) duration of supplemental oxygen therapy among all the subjects recruited

was 26.3(34.5) hours. Table XXI shows that the mean (SD) duration of supplemental oxygen

administration to the subjects with hypoxaemia was 45.1(41.9) hours which was significantly

longer than the corresponding value of 12.9(19.2) hours recorded in those without

hypoxaemia (p=0.001).

The mean duration of oxygen therapy in children with pneumonia increased significantly as

the SpO2 level decreased, p=0.001 (Table XXI). Furthermore, children with severe

pneumonia had supplemental oxygen for a significantly longer mean (SD) duration compared

with the corresponding value in those with moderate pneumonia, p=0.001.

As shown in Table XXI, the mean (SD) duration of the children with lobar pneumonia on

supplemental oxygen was significantly longer at 52.1(55.6) hours compared with the mean

(SD) duration of 21.3(26.3) hours recorded in those with bronchopneumonia, p=0.001. Also,

the mean duration of supplemental oxygen administration to the subjects increased with an

increase in the number of complications, p=0.001 (Table XXI).

76

Table XXI: The duration on oxygen therapy and hypoxaemia in the study population

Parameter n (%) Duration on oxygen (hours) t p-value

Range Mean ±SD

Hypoxaemia

Present 83(41.5) 5-240 45.1±41.9 7.329 0.001

Absent 117(58.5) 0-96 12.9±19.2

Levels of SpO2 (%)

>95 75(37.5) 0-48 5.8±11.9a 17.522* 0.001

93-95 24(12.0) 0-72 20.8±20.6 b

90-92 18(9.0) 0-96 31.9±24.8b,c

86-89 34(17.0) 6-240 47.2±47.8c

≤85 49(24.5) 5-194 43.7±37.9c

Severity of pneumonia

Moderate 12(6.0) 0-72 2.8±9.2 -2.454 0.015

Severe 188(94.0) 0-240 27.8±35.0

Diagnosis

Bronchopneumonia 168(84.0) 0-178 21.3±26.3 -4.869 0.001

Lobar pneumonia 32(16.0) 0-240 52.1±55.6

Admission outcome

Survived 183(91.5) 0-240 26.0±34.4 -0.408 0.684

Died 17(8.5) 5-137 29.5±37.0

Complication

Present 73(36.5) 0-194 41.8±39.2 5.122 0.001

Absent 127(63.5) 0-240 17.3±27.9

Number of complications

None 127(63.5) 0-240 17.3±27.9a 18.000* 0.001

One 52(26.0) 0-98 34.8±27.7b

>One 21(10.5) 0-194 59.2±55.7c

*= F-value (derived from ANOVA) a, b, c: Duncan multiple range test shows that the means with the same letter are not

statistically different at p<0.05.

77

DISCUSSION

The prevalence of hypoxaemia among hospitalized children with pneumonia was estimated to

be 41.5% in the current study which is in accord with the range of 31.0-43.0% found in a

systematic review of hypoxaemia among children with clinical pneumonia by Lozano et al.82

The present value is however lower than the prevalence of 48.0%, 58.9%, and 63.0%

reported from Kenya and the Peruvian Andes.8,83,84 These earlier studies with higher

prevalence values were carried out at high altitudes compared to the location of the present

study which is at near sea level of 303metres.90 Hypoxemia may be more frequent and more

severe in children who live at high altitude because of the reduced pressure of the

atmospheric oxygen. Physiological responses to high altitude hypoxemia comprise shunting

of pulmonary blood flow to the lung apices, an increase in the cardiac output, increase in the

depth and rate of ventilation as well as the pulmonary arterial pressure, exaggerated

vasoconstriction at the lung bases, and a resultant ventilation perfusion mismatch in the

supine position. All of these may further worsen the severity and indeed prolong the duration

of hypoxemia recorded at higher altitude locations.13

Equally noteworthy in the current study is the high prevalence value of 41.5% recorded

among children with severe pneumonia. This value is considerably higher when compared

with the corresponding value of 13.3% (inter-quartile range 7.5-18.5%) reported earlier in

children hospitalized with “severe” and “very severe pneumonia” in a recent systematic

review.7 However, the severity assessment tool of the studies in this recent systematic review

was the WHO clinical classification as against the BTS guidelines (for assessing disease

severity) used in the present study. In areas where facilities for investigations are limited and

there is a paucity of clinicians, health care workers (who may not be doctors) are the first

contact of the patient. Furthermore, these health care workers are trained to identify children

with pneumonia using the WHO criteria for ALRI which does not differentiate between the

78

various ALRI syndromes. There is therefore the possibility of ‘‘diagnostic contaminations’’

by these health personnel who may misdiagnose some AURI syndrome as pneumonia with a

resultant over-diagnosis of the disease. On the other hand, it is also possible to underestimate

the prevalence of severe pneumonia in the poorly organized health services of many

developing countries.46 The implication of this inadequacy in health service delivery is that

many children with severe CAP are not admitted to the hospital, and are therefore more likely

to die at home.46

In the current study, children with lobar pneumonia were found to have a higher prevalence

of hypoxaemia compared to those with bronchopneumonia. However, a valid comparison of

the present data is precluded by the paucity of published studies comparing hypoxaemia in

children with lobar and bronchopneumonia. Lobar pneumonia is associated with more

extensive consolidation of the lungs and hence, a more severe compromise of alveolar

gaseous exchange compared to bronchopneumonia. In lobar pneumonia, there is a reduction

in lung compliance, with extensive loss of functioning lung tissue. The latter may be

attributable to the involvement of one of either a segment or the entire lobe in the

consolidation process and hence, the resultant alveolar hypoventilation and hypoxaemia.5

Also, the resultant hypoxaemia may be attributed to the extensive consolidation which results

in under-ventilated areas of the lungs that are reasonably well perfused with a resultant

ventilation-perfusion mismatch. This is further supported by the fact that bronchial breath

sounds was an independent predictor of hypoxaemia identified in the current study; bronchial

breath sounds are normally heard over an area of lung consolidation which is present in lobar

pneumonia.

Pneumonia remains a serious disease in children and hypoxaemia is reportedly the best

indicator of either or both of a severe and potentially fatal pneumonia.8 Prompt recognition of

hypoxaemia and use of supplemental oxygen therapy improves the outcome in severe

79

pneumonia.89 The current study had examined the association between some clinical features

of children with pneumonia and the SpO2 levels with the aim of identifying their usefulness

as early predictors of hypoxaemia. Restlessness, inability to drink, lethargy, difficult

breathing, cyanosis, pallor, grunting, intercostal recession, lower chest wall in-drawing,

bronchial breath sounds and tender hepatomegaly were significantly associated with

hypoxaemia in the present study. With the exception of pallor, previous studies had also

identified these clinical findings as significant predictors of hypoxaemia.11,13,14,16,84,95

However, in the present study some of these clinical features with high sensitivity had poor

specificity and vice versa. This observation is in accord with the findings in earlier

studies.11,13,14,16,84,95 The wide variability in the sensitivity and specificity of the symptoms

and signs reported in predicting the presence of hypoxaemia could be due to differences in

definitions of hypoxaemia used, even among studies conducted at similar altitudes. While

Onyango et al 8 defined hypoxaemia as SpO2< 91%, Dyke et al85 defined same as SpO2<

86% while a SpO2< 88% was used by Duke et al.86

The best clinical predictors for detecting hypoxaemia in the current study are the presence of

restlessness, lower chest wall indrawing, bronchial breath sounds and tender hepatomegaly.

Restlessness, as a manifestation of impaired mental state, has been shown to have a very

close correlation with oxygen saturation, and the degree of restlessness tends to increase with

increasing hypoxaemia.11 Thus, its presence should arouse the suspicion of both the clinician

and the health worker of the presence of hypoxaemia. While restlessness was a significant

finding in the present study, which is similar to the findings in an earlier report from the

Gambia,9 it was not associated with hypoxaemia in another study.10

Previous studies that examined the relationship between chest indrawing and hypoxemia had

conflicting results.8,9,14,16,84 In one of these studies which was carried out at high altitude,8

chest indrawing was reportedly highly sensitive (88%) but poorly specific. This observation

80

is in accord with that of the present study. On the other hand, other workers had reported

variable sensitivity (35.0-78.5%) but a high specificity (60.0-94.0%) respectively.9,14,16,84

However, chest indrawing was the best independent predictor of hypoxaemia in the present

study, and this appears to be consistent with the findings from some earlier studies.8,16 Lower

chest indrawing is an evidence of severe respiratory distress with increased respiratory

muscle effort and increased work of breathing in an attempt to breathe against a poorly

compliant lung parenchyma. The clinical implication of the current finding is that the absence

of this sign is only likely to miss a small percentage of patients with pneumonia who are

hypoxemic.

Several studies have found the association of auscultatory signs such as crepitations or

rhonchi to be associated with hypoxaemia.10,83,85 On the other hand, others did not find a

consistent association between the presence of these auscultatory signs and hypoxaemia.9,84

The finding in the present study of a significant association between bronchial breath sound

and hypoxaemia with a high specificity and poor sensitivity is noteworthy. However, a valid

comparison with previous work is precluded by the paucity of comparable reports on the

study. The fact that BBS is associated with hypoxaemia may be explained by the fact that

BBS is usually heard over consolidated area(s) of the lung. This pathologic change is more

likely to be accompanied by ventilation-perfusion mismatch, alveolar hypoventilation and a

resultant severe hypoxaemia.

The current study found that tender hepatomegaly had a fair sensitivity but a moderate

specificity, PPV and NPV. The presence of tender hepatomegaly, tachypnoea and tachycardia

in a child with pneumonia remains a valid clinical indicator of heart failure.24 The

predominance of heart failure as a complication of childhood pneumonia in the current study

is consistent with the findings of earlier Nigerian hospital-based reports.4,24,74 The high

prevalence of heart failure in the current series is not surprising, especially in view of the

81

significant inflammation-driven reduction in the lung compliance associated with

pneumonia.24 Consequently, heart failure may occur due to the resultant right ventricular

strain.24 A prompt identification and treatment of co-morbid heart failure remains a crucial

aspect of the management of childhood pneumonia. In this regard, identification of heart

failure as a predictor of hypoxaemia should hardly pose a problem for the clinician in view of

the ease of identifying the clinical parameter of liver tenderness.

Oxygen administration remains the key therapeutic measure in children with hyoxaemia. A

judicious deployment of this important “medication” by administering the agent to patients

who need it remains a desirable cost-saving measure in health care service delivery. Against

this background, the implication of the low sensitivity of various signs of hypoxemia in a

clinical setting is that some children with severe pneumonia who need oxygen will not

receive it if the administration is based on clinical evaluation alone.96 However, therapy

based on clinical signs with high sensitivity but at the same time low sensitivity is likely to

encourage the hardly cost-effective and inappropriate administration of oxygen. This

resource (oxygen) is often expensive and in limited supply in low income countries.96

Clearly, it is this logic that underscores the value of pulse oximetry as a cost-effective

intervention in small and moderate sized hospitals in developing countries.80,97 As shown by

the present study, the use of the pulse oximeter (as against the more hazardous and more

expensive measurement of arterial blood gases) has proven to be an invaluable and safe bed

side investigative tool for detecting pneumonia-related hypoxaemia.

Various risk factors which were earlier identified with the occurrence and severity of

pneumonia were explored as possible clinical correlates of hypoxaemia in the current study.

In this regard, hypoxaemia was found to be associated with a low socio-economic

background of the child, high birth order of the child, low maternal age, poor maternal

literacy level, as well as a poor immunization status.

82

As is the case with most of the risk factors explored, the dearth of earlier published data on

the association between risk factors of pneumonia and the presence of hypoxaemia would

obviously preclude a robust comparison with previous data. However the current association

of low socio-economic background with hypoxaemia is putatively attributable to parental

health-seeking behaviour; the more affluent, literate mothers are more likely to afford and

seek health care early and hence, their chidren’s illness more likely to be less severe, and the

risk of hypoxaemia lower.98

Similarly, the appropriate and timely health care-seeking behaviour, as well as a clear

understanding of the available preventive strategies are less likely to be appreciated by the

younger, illiterate mothers.99 In such children with a poor parental socio-economic

background, the (expected) inadequate family income would hardly support a prompt and

appropriate health seeking behaviour in the event of the occurrence of pneumonia.98 One of

the possible consequences of such belated presentations (at the relevant health care facilities)

is the unfettered progression of the pneumonia with increasing risk of hypoxemia. Also,

children from higher socioeconomic class are more likely to be better nourished and thus

protected from severe pneumonia and its severe complications. However, the current study

did not however find any association between a poor nutritional status (as a risk factor of

pneumonia) and the presence of hypoxaemia.

The finding of a higher proportion of hypoxaemia in children of high birth order compared to

the corresponding observation in those with a low birth order in the current study is not

surprising. Birth order has been reported to be a risk factor for pneumonia.2 A high birth

order suggests that there is an increased likelihood of a higher number of siblings/other

children in the household sharing the meager household facilities and food, and are therefore

exposed to a higher risk of overcrowding and malnutrition. This may be further aggravated

83

by short birth intervals between the siblings in the household such that the maternal care is

inadequate. The predisposition of the child of high birth order to severe pneumonia with

resultant hypoxaemia may be a consequence of some or all of these aforementioned adverse

household variables.

Measles and pertussis are vaccine preventable co-morbidities which had earlier been

identified with pneumonia-related deaths.25 The present study found that a poor immunization

status (as a co-morbidity of pneumonia) was associated with a higher risk of hypoxaemia. In

addition, there was a negative correlation between lack of immunization and the presence of

hypoxaemia such that the children who were unvaccinated were at increased risk of having

hypoxaemia. Appropriate immunization in childhood has been shown to confer protection

against pathogens that could cause severe pneumonia.2,62, 100 Therefore, unvaccinated children

are more likely to have no protection against these pathogens, develop severe pneumonia and

thus an increased risk of hypoxaemia.

The relevant correlation values of all the aforementioned risk factors of pneumonia with

respect to hypoxaemia is however weak, and there is therefore a need for a larger series. Also

noteworthy for its absence in the present study is the earlier reported association between age

of the children with pneumonia and the occurrence of hypoxaemia. Earlier reports from

India13 16had suggested that hypoxaemia was significantly more common in infants compared

with older children.

Hypoxaemia was present in a higher percentage of the children with bacteraemia compared

with the corresponding value in those without bacteraemia. While this finding was not

significant in the present study, it is apparently in accord with those of Nantanda et al in

Uganda.81 The most common bacterial pathogen of pneumonia in the current study was

Staphylococcus aureus, a finding that is similar to the earlier findings from Ibadan,45 Ilorin,4

Benin,77and Uganda.81 Although Streptococcus pneumoniae and Haemophilus influenzae type

84

b are reportedly the most common bacterial pathogens worldwide,2 this was not the case in

the current study. The absence of these two key organisms of pneumonia, Streptococcus

pneumoniae and Haemophilus influenzae, from the spectrum of the isolates may be a

reflection of the limited microbiologic support for the isolation of these organisms at the

current study site. However, the present study was not designed to identify a possible

association of the individual bacterial pathogens with the presence of hypoxaemia in the

children studied.

The case fatality among the children with pneumonia in the current series was 8.5%. While

this value is slightly higher than the 7.8% recorded by Johnson et al in Ibadan,24 a slightly

higher case fatality value of 10.0% had been identified in an earlier report (some 25years

earlier)4 from Ilorin where the present study was carried out. The corresponding values from

other countries included the 15.0% reported by Nathoo et al 100 in Zimbabwe and 10.5% by

Seghal et al54 in India. None of these values was lower than the recorded value in the present

study. The small, but hardly significant decrease in pneumonia-related mortality over the

years in the present study may be possibly ascribed to a more prompt home recognition of

disease severity, early diagnosis, better defined criteria for referrals, as well as the

institutional adoption of more effective management strategies in the last few years.46,54

The fact that the presence of hypoxaemia was associated with a significantly higher

pneumonia-related mortality is in accord with the findings in earlier reports.8,10,12,81 Majority

of the children might have had pre-admission antimicrobial therapy which could have been

either inappropriate or not completed due to cost considerations. The consequence of this is a

severe disease or a fatal outcome possibly due to drug-resistant pathogens. Also, the

association of a higher fatal disease outcome with hypoxaemia may be ascribed to a

prolonged pre-admission duration of this complication due to parental delay in seeking

hospital consultation. While there is a paucity of published studies documenting the

85

relationship between the presence of pneumonia-associated complications and hypoxaemia,

the current study was able to show that hypoxaemia was more common in children with

pneumonia-associated complications compared to those without any complications. Indeed,

the lower the SpO2 levels, the more the number of complications and the higher the mortality.

Similarly, the presence of hypoxaemia had earlier been associated with severe pneumonia.46

Hence, it can be safely deduced that the presence of pneumonia-related complications is a

marker of disease severity.88 Clearly, a timely recognition of pneumonia complications, as

well as prompt institution of specific therapy remain indispensable components of a

favourable treatment outcome of the disease.

In the present study, the duration of hospital stay was found to be significantly longer for

hypoxaemic children compared with the corresponding value in non-hypoxaemic children.

This observation is similar to the reported findings in some earlier studies.8,10 Indeed, the

mean duration of hospitalization increased as the levels of hypoxaemia worsened with

decreasing SpO2 levels. This apparent inverse relation between the SpO2 levels and the mean

duration of hospitalization was significant. A possible explanation for this relationship

appears to be the longer time required by hypoxaemic children with pneumonia to recover

from the underlying pathophysiological aberrations of alveolar hypoventilation and

ventilation-perfusion mismatch.

Children with lobar pneumonia (LP) had a longer mean duration of hospital stay which was

approximately twice that of the corresponding value in those with bronchopneumonia (BP).

This current finding is similar to the observation made in an earlier report by Johnson et al.74

The more extensive area of consolidation in lobar pneumonia may be associated with a more

severe ventilation-perfusion mismatch and alveolar hypoventilation and hence, a more severe

level of hypoxaemia. Also, this finding could be related to the fact that BP may be attributed

to a greater likelihood of a viral aetiology, as against a bacterial aetiology in LP.2,46,74

86

Complete and rapid resolution is the rule in most cases of viral pneumonia as against the

expected slower resolution in the extensive lobar consolidation with LP and bacterial

aetiology.2,46,74

In the current study, the presence of pneumonia-related complications was associated with a

longer mean duration of stay (approximately twice) compared to those without complications.

A possible explanation include the fact that the children with pneumonia-related

complications would need a longer time to recover from both the pneumonia and the

complication(s) as against the expected faster resolution in children with uncomplicated

pneumonia. Hence, the current findings with respect to pneumonia-related complications

constitute compelling grounds for a timely recognition and treatment of complications at

presentation.

Supplemental oxygen is given to children with pneumonia to relieve hypoxaemia. In the

present study, the mean duration of treatment with supplemental oxygen administration

increased with decreasing SpO2 and severity of pneumonia. Furthermore, children with

pneumonia-related complications had a longer mean duration of treatment with supplemental

oxygen (2.5 times) when compared those with uncomplicated disease. In addition, children

with multiple pneumonia-related complications had significantly longer duration on

supplemental oxygen. In most centres in developing countries including Nigeria, hospital-

based facilities for continuous monitoring of SpO2 levels are not available for all patients that

require oxygen therapy. Hence, the inevitable need for rationing this therapy frequently

informs the discontinuation of the oxygen administration with the earliest evidence of clinical

resolution of respiratory distress. Also, this study has shown that without monitoring the

SpO2 levels, there is a small but definite tendency to initiate oxygen therapy in children with

SpO2 levels that are within normal range. Clearly, this constitutes a potential source of

87

oxygen wastage, with the subsequent non-availability for patients that require this life saving

treatment measure. This data therefore underscores the need to make pulse oximeters

available in our health care facilities, with the capacity and wherewithal for administering

oxygen therapy.

In conclusion, the identified prevalence of pneumonia-associated hypoxaemia is high in the

present study population. It has also been identified that the best independent clinical

correlates of hypoxaemia are restlessness, the presence of lower chest wall indrawing,

bronchial breath sounds and tender hepatomegaly. For clinicians working at the higher tiers

of health care delivery, the presence of chest wall indrawing, lobar consolidation and clinical

evidence of heart failure should arouse a high index of suspicion for hypoxaemia in the

patient. The identification of these clinical parameters in a child with pneumonia should also

dictate the need for supplemental oxygen in an emergency room setting even when the SpO2

cannot be monitored. On the other hand, for the health care workers at the primary health care

facility, lower chest wall indrawing remains perhaps the single most reliable clinical predictor

of hypoxaemia that should suggest a need for immediate referral to centres where oxygen

therapy is available.

88

CONCLUSIONS

The following conclusions can be drawn from the present study:

1. The prevalence of hypoxaemia in the children with pneumonia was 41.5%

2. The best independent clinical predictors of hypoxaemia identified were restlessness,

lower chest wall indrawing, bronchial breath sounds and tender hepatomegaly.

3. Low socio-economic class of the child, high birth order of the child, low maternal age

and maternal literacy level, as well as poor immunization status were risk factors of

pneumonia significantly associated with the presence of hypoxaemia.

4. The presence of pneumonia-related complications, especially heart failure was

associated with hypoxaemia.

5. Mortality and the pneumonia-associated complications were higher in hypoxaemic

children compared with their non-hypoxaemic peers.

6. The mean SpO2 level was lower amongst the fatal cases compared with the value in

the survivors.

7. Duration on supplemental oxygen therapy increased with increasing level of

hypoxaemia and there is an apparent need for concomitant pulse oximetry monitoring

in patients on oxygen therapy to reduce wastage.

89

RECOMMENDATIONS

The following recommendations have been made based on the study:

1. Pulse oximeters should be made available in various hospitals and monitoring for

hypoxaemia should be included in the guidelines for the routine inpatient

management of children with severe pneumonia.

2. The presence of lower chest wall indrawing, bronchial breath sounds and clinical

heart failure in children with pneumonia may be used by clinicians as an index of

adjudging the presence of hypoxaemia in areas where pulse oximeters are not

available.

3. The health care workers at the primary health care facility may use restlessness and

lower chest wall indrawing as a predictor of hypoxaemia. These features should serve

as an urgent sign for referral to centres where oxygen therapy is available.

90

LIMITATIONS OF THE STUDY

1. Continuous pulse oximeter monitoring would have been the ideal for the present study

as against the intermittent use of the device in the study.

2. Bactec is the ideal way of doing bacterial blood culture which was however not

available at health facility where the current study was carried out.

3. Determination of arterial blood gases is the ‘gold standard’ for measuring the partial

pressure of oxygen which could not be carried out in the present study.

91

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APPENDIX I

CLINICAL PREDICTORS OF HYPOXAEMIA IN CHILDREN AGED TWO

MONTHS UP TO FIVE YEARS WITH PNEUMONIA AT THE UITH, ILORIN

INFORMATION SHEET FOR PARENTS/CAREGIVERS OF PROSPECTIVE

SUBJECTS

WHAT IS THE STUDY ABOUT?

The study is intended to find out how common low blood level of oxygen (low arterial

hemoglobin saturation or hypoxaemia) is in patients with pneumonia, the clinical symptoms

and signs associated with it and the outcome of hypoxaemia in Nigerian children aged two

months to five (5) years, seen at the Emergency Paediatric Unit (EPU) of the University of

Ilorin Teaching Hospital.

BENEFIT(S) OF PARTICIPATION

Observations made at the end of this study will contribute to the understanding of the various

symptoms and signs that are associated with hypoxaemia in patients with pneumonia and thus

aid in the early recognition of this lethal complication, as well as the need for early

commencement of oxygen treatment. It would also ensure that wastage of oxygen is

minimized.

POTENTIAL RISK(S) OF PARTICIPATION

The only anticipated risk is the discomfort of putting the pulse oximeter gadget on either the

toe or the finger. There is definitely no risk of damage to the fingers or toes.

WHAT IS EXPECTED OF YOU IF YOU AGREE TO PARTICIPATE?

You will be expected to provide answers to simple questions like your child’s age, sex, your

level of education and occupation which are in any case required for making the right

diagnosis and as well as starting the correct treatment in the first place. Your child will then

be examined in detail, and the arterial oxygen saturation will be taken using a pulse oximeter.

103

However, your child will still have other tests required for making the right diagnosis and

formulating the right treatment, all of which would have been done, regardless of

participation in the study. These include chest radiographs and a few blood tests.

CONFIDENTIALITY!

The information obtained will be treated in absolute confidence. No part or whole of such

information shall be divulged to anyone except the investigators. We owe it a duty to keep

your child’s records absolutely confidential.

YOUR PARTICIPATION IS VOLUNTARY!

Your participation and that of your child are voluntary. You may withdraw him/her at any

time in the course of the study. Please note that your participation or refusal (to participate)

will in no way influence the quality of treatment and care given to your child or ward.

COST OF PARTICIPATION

The measurement of arterial oxygen saturation, examination of the child and completion of

questionnaires attract no cost; the cost of your participation in this study is absolutely free.

This is however exclusive of the cost of routine investigations and treatment.

104

APPENDIX II

INFORMED CONSENT FORM

Alhaji/Hajia/Chief/Mr/Mrs ……………………………….....……………………..

Whose address is ……………………….....………………….....…………. do hereby gives

consent on behalf of my child or ward to participate as a subject in a study/research as

explained to me verbally and as contained in the attached “Information sheet for Parents &

Care givers.” I am aware that my child will be fully evaluated and treated regardless of my

consent or otherwise to participate in the study.

All the terms of this consent including the potential risks and what it takes to participate have

been fully explained to me in a language that I understand.

Signature/thumbprint__________________

Signature________________________

Child’s Parent/Guardian Interviewer

Date_________________________________

Time__________________________________

Witness’s signature:_____________________

Name of witness:______________________________

105

APPENDIX III: STUDY PROFOMA

CLINICAL PREDICTORS OF HYPOXAEMIA IN CHILDREN AGED TWO

MONTHS UP TO FIVE YEARS WITH PNEUMONIA AT THE UITH, ILORIN

Hospital No_________Serial No _______ Name____________________________

Date of Presentation____________ Informant _______________

A) Sociodemographic data

1. Age________

2. Sex: Male (1) Female (2)

3. Mother’s Education level: university/HND(1) post secondary(2) secondary(3)

primary (4) none (5) arabic(6) not known (7)

4. Father’s Education Level: university/HND(1) post secondary(2) secondary(3)

primary (4) none (5) arabic(6) not known (7)

5. Mother’s Occupation: …………. professionals(1) senior school teacher or its

equivalents(2) Junior school teachers, drivers, artisan(3) petty trader(4)

housewife/unemployed(5) student(6) not known/dead(7)

6. Mother’s age :_________________________________

7. Father’s Occupation: professionals(1) senior school teacher or its equivalents(2)

Junior school teachers, drivers, artisan(3) petty trader(4) unemployed(5)

student(6) not known/dead(7)

8. Family type : Monogamous (1) Polygamous (2)

9. No. of sibling(s): 1-2 (1) 3-4 (2) ≥5 (3) none (4)

106

10. Birth order: With respect to mum_______________ With respect to

dad_______________

11. Birth interval: 1st birth(1) <24mths(2) 24-35mths(3) >36mths(4)

12. Does anyone in the household smoke: yes(1) no (2) not known(7)

13. If yes, who? Father(1) mother(2) siblings(3) neighbours(4)

aunt/uncle(5) grandparent(6) mixture(7)

14. If yes, does the child sleep in the same room with the smoker:

Yes(1) No(2) not known (7)

15. Where does cooking take place? Inside the room(1) Corridor inside the house(2) Kitchen

in the house(3) Open space/backyard(4)

16. Facilities for cooking: electricity(1) Firewood(2) kerosene(3)

gas(4) charcoal(5) combination(specify)__________(6) Not known(7)

17. Attendance at day care center: Yes(1) No(2) not known (7)

18. Any immunization: Yes(1) No(2) not known (7)

Vaccine BCG HBV OPV DPT Measles Yellow fever

1st 2nd 3rd 1st 2nd 3rd 4th 1st 2nd 3rd

Yes(1)

No(2)

Not due yet (3)

Not known(7)

19. Type of food before introduction of solids (pre-weaning):

breast milk only(1) infant formula only(2) mixed(3)

20. If breastfed only, duration of exclusive breastfeeding:

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<3months(1) 4 – 6 months(2) none (3) not known(7)

21. PRESENT ILLNESS HISTORY

A) Non respiratory symptoms

Symptom Present (1)/Absent(2) Duration(days}

1. Fever

2. Inability to feed

3. Inability to drink

4. Restlessness

5. Lethargy

6. Vomiting

7. Diarrhea

8. Rash

9 .Others(specify)

B) Respiratory symptoms

Symptom Present (1)/Absent(2) Duration(days}

1. Cough

2. Nasal discharge

3. Difficulty breathing

4. Fast breathing

5. Wheeze

6. Chest pain

7.Others(specify)

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23. GENERAL PHYSICAL EXAMINATION

a) Anthropometric measurement

Weight_____________ Expected weight for age_________%

Height _____________Mid-Upper Arm Circumference _______________

b) Hydration status: well hydrated (1) mild dehydration (2)

moderate dehydration(3) severe dehydration (4)

c) Pallor (Y/N) ________________________________

d) Axillary temperature recording (oC) _______________________

e) Oedema Yes (1) No (2)

24. RESPIRATORY SIGNS

a. Respiratory rate per minute _____________________________

b. Central cyanosis: Yes (1) No (2)

c. Grunting: Yes (1) No (2)

d. Wheeze: Yes (1) No (2)

e. Snuffles/noise from blocked nostrils: Yes (1) No (2)

f. Rhinorrhoea: Yes (1) No (2)

g. Nasal flaring: Yes (1) No (2)

h. Intercostal recession: Yes (1) No (2)

i. Lower chest wall indrawing: Yes (1) No (2)

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j. Percussion notes: normal (1) dull (2) hyperresonant (3)

k. Breath sounds: normal (1) diminished (2) absent (3)

l. Bronchial breath sounds: Yes (1) No (2)

m. Adventitious sounds: crepitations (1) rhonchi (2)

none (3) crepitations and rhonchi

(4)

n. Head nodding Yes (1) No (2)

p. Other respiratory findings (specify)___________________________________

_________________________________________________________________

25. OTHER SYSTEMIC FINDINGS

Heart rate_________________________________________________________

Heart sounds______________________________________________________

Hepatomegaly : Yes(1) No(2)

If yes, any tenderness: Yes (1) No (2)

Splenomegaly : Yes(1) No(2)

Unconscious: Yes(1) No(2)

If yes, GCS score_____________________________

Other findings_____________________________________________________

_________________________________________________________________

_____________________________________________________________________

____________________________________________________________________

26. DIAGNOSIS: bronchopneumonia (1) lobar pneumonia(2) mixed(3)

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o COMPLICATIONS: Yes (1) No(2)

o If yes, indicate type:_____________________________________________

Severity of pneumonia_____________________________________________

27. RESULTS

Pulse Oximeter Reading_______________________________________

Pulse oximeter reading on O2_____________________________________________________

HYPOXAEMIA: Yes(1) No(2)

Chest radiograph findings_____________________________________

_____________________________________________________________________

_____________________________________________________________________

____________________________________________________________________

Haematocrit/packed cell volume______________________________

Total WBC count_________________________________________

WBC Differentials____________________________________________

__________________________________________________________________

_________________________________________________________________

Blood Culture growth: Yes(1) No(2)

If positive, indicate organism_____________________________________

28. OUTCOME OF ADMISSION:

a. recovery(1) death(2) DAMA(3)

b. duration of hospitalization_____________________________

c. duration on supplemental oxygen therapy_____________________

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APPENDIX IV

SOCIAL CLASSIFICATION SCHEME

SOCIAL

CLASS

PROFESSION EDUCATIONAL

ATTAINMENT

I Professional, Senior Public Servants, Owners of

large business concerns, Senior military officers,

large-scale contractors.

University graduates or

equivalents

II Non-academic professional e.g. Nurses, Secondary

school teachers, Secretaries, Owners of medium

sized business, intermediate grade public servants.

School certificate holders

and equivalent

III Non-manual skilled workers including clerks,

typist, telephone operators, junior school teachers,

driver.

Grade II teachers or

equivalent

IV Petty traders, Labourers, Messengers Primary certificate

V Unemployed. Full time house wives, students,

subsistence farmers.

No formal education

The mean of four scores (two for the father and two for the mother) to the nearest whole

number is the social class to be assigned to the child.

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APPENDIX V

Severity assessment of pneumonia according to British Thoracic Guidelines

Mild to moderate Severe

Infants Temperature <38.5°C Temperature >38.5°C

RR <50 breaths/min RR >70 breaths/min

Mild recession Moderate to severe recession

Taking full feeds Nasal flaring

Cyanosis

Intermittent apnoea

Grunting respiration

Not feeding

Tachycardia(age dependent)

Capillary refill time > 2seconds

SpO2 <92%

Older Children Temperature <38.5°C Temperature >38.5°C

RR <50 breaths/min RR >50 breaths/min

Mild breathlessness Severe difficulty in breathing

No vomiting Nasal flaring

Cyanosis

Grunting respiration

Signs of dehydration

Tachycardia (age dependent)

Capillary refill time > 2 seconds

SpO2 <92%

Significant tachycardia - HR > 160beats/minute in infancy; >150 beats/minute at 1year;

>140beats/minute at 2 years; 130beats/minute at 3 years; 120 beats/minute at 4 years and

>110beats/minute at 5 years

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APPENDIX VI

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APPENDIX VII