ENLARGED ADENOIDS AND CARDIORESPIRATORY
COMPLICATIONS IN CHILDREN AT LADOKE AKINTOLA
UNIVERSITY OF TECHNOLOGY (LAUTECH) TEACHING
HOSPITAL, OSOGBO
BY
DR TAIWO OLUGBEMIGA ADEDEJI MBChB (Ife)
DEPARTMENT OF OTORHINOLARYNGOLOGY LADOKE
AKINTOLA UNIVERSITY OF TECHNOLOGY TEACHING
HOSPITAL, OSOGBO, OSUN STATE, NIGERIA
A DISSERTATION SUBMITTED TO THE NATIONAL POSTGRADUATE
MEDICAL COLLEGE OF NIGERIA IN PARTIAL FULFILLMENT OF THE
REQUIREMENTS FOR THE AWARD OF FELLOWSHIP OF THE NATIONAL
POSTGRADUATE MEDICAL COLLEGE OF NIGERIA IN
OTORHINOLARYNGOLOGY (F.M.C.ORL)
MAY, 2012
i
DECLARATION
I, DR TAIWO OLUGBEMIGA ADEDEJI, do hereby declare that this dissertation is original and the research carried out by me. The dissertation has not been presented to any College for
Fellowship examination nor submitted elsewhere for publication.
……………………………………… ………………………….
Dr Taiwo Olugbemiga Adedeji Date
ii
CERTIFICATION
This is to certify that the work of this dissertation:”Enlarged adenoids and cardiorespiratory complications in children” has been carried out by Dr Taiwo Olugbemiga ADEDEJI of the department of Otorhinolaryngology, Ladoke Akintola University of Technology Teaching
Hospital, Osogbo, under our supervision.
First Supervisor DR (Mrs) Y B AMUSA …………………………………….
Signature
Second Supervisor PROF GTA IJADUOLA …………………………………….
Signature
Third Supervisor DR AA AREMU …………………………………..
Signature
iii
ACKNOWLEDGEMENT
My gratitude goes to my supervisors; Dr (MRS) YB AMUSA, Associate Professor and
Consultant Otorhinolaryngologist, Obafemi Awolowo University Teaching Hospital, Ile Ife,
Professor GTA IJADUOLA Professor and Consultant Otorhinolaryngology University College
Hospital, Ibadan and Dr AA AREMU, a Consultant Radiologist LAUTECH Teaching Hospital,
Osogbo who worked tirelessly and supervised this project painstakingly.
I acknowledge with thanks the efforts of Dr. OA Olaosun, Consultant Otorhinolaryngology,
LAUTECH Teaching Hospital, Osogbo for his invaluable advice and contributions in the course of this project. Special appreciation goes to Dr AA Akintunde a Consultant Cardiologist
LAUTECH Teaching Hospital, Osogbo who helped to review the Electrocardiogram (ECG) of the patients. I appreciate the efforts of Drs DG Oyedemi, and E Agedebe of Department of paediatric. Special thanks to Mrs RT Iyiola and Mrs TA Oyekale of ECG unit of Department of medicine and Mr BA Ayanlola of Department of Radiology. I also acknowledge Dr AA Hastrup and fellow residents, nurses and other departmental staffs of the department of
Otorhinolaryngology LAUTECH Teaching Hospital, Osogbo.
Special appreciation goes to my head of department Dr JE TOBIH for his encouragement and fatherly advice.
I am grateful to my wife Olukemi for her support, prayer and encouragement and to my children
David, Inioluwa and Obaloluwa. Finally I give all the glory to God Almighty who has made this work a reality.
iv
DEDICATION
This work is dedicated to the Almighty God, the giver of life who has always been with me even throughout the period of my training.
v
TABLE OF CONTENTS
Title page i
Declaration ii
Certification iii
Acknowledgement iv
Dedication v
Table of contents vi
List of tables ix
List of figures xi
Key of abbreviations xii
Summary xiii
Chapter 1
Introduction 1
1.1 Background 1 1.2 Epidemiology 3 1.3 Justification for the study 3
Chapter 2
Aims and objectives 5
Chapter 3
Literature review 6
3.1 Pathogenesis of obstructive sleep apnoea in children with enlarged adenoid 6
vi
3.2 Pathogenesis of cardiovascular diseases in patients with enlarged adenoid 7
3.3 Cardiorespiratory findings 8
3.4 Radiology of adenoids 9
3.5 Electrocardiographic (ECG) features 11
3.6 Other causes of cardiopulmonary morbidities and mortalities 11
Chapter 4
Methodology 13
4.1 Study design 13
4.2 Study location 13
4.3 Sample size determination 13
4.4 Inclusion criteria 14
4.5 Exclusion criteria 15
4.6 Patients and methods 15
4.7 Data analysis 17
4.8 Ethical consideration 18
Chapter 5
Results 19
Chapter 6
Discussion 37
Conclusion 42
Recommendation 43
vii
Benefit of the study to participants, science and knowledge 44
Limitations 44
References 45
Appendix 1 53
Appendix 2 55
Appendix 3 56
Appendix 4 57
Appendix 5 58
Appendix 6 59
Ethical clearance certificate 60
National Postgraduate Medical College of Nigeria Approval Letter 62
viii
LIST OF TABLES
Table 1 Age distribution of subjects and controls 19
Table 2 Gender distribution of subjects and controls 20
Table 3 Distribution of symptoms and signs of adenoid enlargement 22
Table 4 Distribution of adenoidal nasopharyngeal ratio of the subjects 24
Table 5 Association between adenoidal nasopharyngeal ratios and age group 25
Table 6 Association between adenoidal nasopharyngeal ratios and gender 26
Table 7 Electrocardiographic findings among the subjects 27
Table 8 Pattern of ECG abnormalities among the subjects and the controls 28
Table 9 Prevalence of chest infections among the subjects and the controls 29
Table 10 Association between ECG findings and adenoidal nasopharyngeal ratio 30
Table 11 Association between ECG findings and age of the subjects 31
Table 12 Association between gender and ECG findings among the subjects 32
Table 13 Association between ECG findings and duration of illness among the
subjects 33
Table 14 Association between chest infection and adenoidal nasopharyngeal ratio
among the subjects 34
ix
Table 15 Association between chest infection and age of the subjects 35
Table 16 Association between cardiomegaly and adenoidal nasopharyngeal ratio 36
x
LIST OF FIGURES
Figure 1 Bar chart showing age prevalence among the subjects and the controls 21
Figure 2 Pie chart showing children with failure to thrive and chest wall deformity 23
xi
KEY OF ABBREVIATIONS
ANOVA One way analysis of variance
ANR Adenoid nasopharyngeal ratio
BVH Bi ventricular hypertrophy
CT Computerized tomography
CXR Chest x – ray
ECG Electrocardiography
ENT Ear, Nose and Throat
IgA Immunoglobulin A
IgG Immunoglobulin G
LVH Left ventricular hypertrophy
LAE Left atrial enlargement
MRI Magnetic resonance imaging
PaCO2 Partial pressure of carbon dioxide
PaO2 Partial pressure of oxygen
RVH Right ventricular hypertrophy
SD Standard deviation
VEGF Vascular endothelial growth factor
VSD Ventricular septal defect
X2 Chi square
xii
SUMMARY
Adenoids are aggregates of lymphoid tissue under the mucosa of the nasopharynx. They form part of Waldeyer’s ring of lymphoid tissue at the portal of the upper respiratory tract, the nasopharynx. It is also one of the important sites of contact of inhaled microorganism and antigens with immunoactive cells. When adenoids become grossly enlarged they may predispose to cardiorespiratory abnormalities with its attendant morbidity. This study aims to find out pattern and prevalence of cardiorespiratory complications in children with enlarged adenoids and any other associated problems in them
It was a cross sectional, hospital – based study. It involved subjects who had been thoroughly assessed by me for history, clinical and radiological evidence of enlarged adenoids. The chest radiographs and electrocardiograph (ECG) were carried out and reviewed by me first and then with consultant Cardiologist and Radiologist with joint findings correlated. Data collected was analyzed with statistical package for social sciences (SPSS) version 14.0 windows (SPSS Inc,
Chicago, II, USA) software package.
There were 90 subjects and 90 controls, male: female ratio 2.1: 1, peak age group of presentation was 12 to 35 months. Abnormal ECG was found in 16.7% while 24.4% had chest infection. Left ventricular hypertrophy, right ventricular hypertrophy and bi-ventricular hypertrophy with left atrial enlargement were the common abnormalities. Non cardiorespiratory findings were failure to thrive (11.1%) and chest wall deformity (4.4%). Severity of obstruction of the nasopharynx by adenoids had correlation with cardiorespiratory complications
Key words: Enlarged adenoids, cardiorespiratory complications, electrocardiography, chest x- ray.
xiii
CHAPTER 1
INTRODUCTION
1.1 Background
Adenoids are aggregate of lymphoid tissue under the mucosa of the nasopharynx. They are covered by pseudostratified ciliated columnar epithelium rich in goblet cells plicated to form numerous surface folds which increase the surface area. Nasopharyngeal lymphoid aggregates were first described by Santorini in 1724 and not until 1870 was the term Adenoids coined by Wilhelm
Mayer1.
Adenoids together with peritubal lymphoid tissue, palatine and lingual tonsils form Waldeyer’s ring of lymphoid tissue at the portal of the upper respiratory tract1, hence, it is an important site of contact of inhaled microorganisms and antigens with immunoactive cells.
Lymphoid tissue that forms adenoids can be identified at 4-6 weeks gestation lying within mucous membrane of the roof and posterior wall of the nasopharynx and this may extend to the fossa of
Rosenmuller and to Eustachian tube orifice as tubal tonsil. Adenoids can be identified by magnetic resonance imaging (MRI) at age of 4 months in 18% of children2. At age 5 months, it could be identified in most children1, 2. It enlarges from infancy through adolescence in most children and thereafter decreases in size3. Upper airway soft tissues including the adenoids grow more rapidly than the bony structure of the nasopharynx from three to five years of age with consequent decrease in size of the airway during this period hence clinical symptoms are more common in the younger age group due to relative small volume of the nasopharynx and the increase frequency of upper respiratory infections3, 4and5. Adenoids receive rich blood supply from branches of the facial and maxillary arteries and the thyrocervical trunk. Venous drainage is to the internal jugular and facial
1 veins. Lymphatic drainage is to the retropharyngeal and upper deep cervical nodes. Nerve supply is from sensory branches of glossopharyngeal and vagus nerves.
Adenoids produce B cells which give rise to five types of immunoglobulin but immunoglobulin G
(IgG) and immunoglobulinA (IgA) are the most important products1, 6. Exposure to antigens via the nasal route is an important part of naturally acquired immunity in childhood1. Enlarged adenoids resulting from response to infection or allergy have been implicated in upper respiratory tract disease causing partial or complete nasopharyngeal airway obstruction1. These effects subsequently lead to various pathological manifestations which include otitis media with effusion, rhinitis, rhinosinusitis, adenoiditis, obstructive sleep apnea and anosmia/ hyposmia1. Clinically, children with adenoidal obstruction present with recurrent nasal discharge, mouth breathing, stertorous breathing, hyponasal speech, obstructive breathing during sleep, restlessness and excessive daytime sleepiness1.
Various studies have shown that enlarged adenoids are associated with cardiorespiratory abnormalities with its attendant morbidity and mortality7, 8, 9 and10. Tal et al.8 reported that obstructive sleep apnea in children is almost always caused by enlarged adenoids and are cured by its removal.
Greenfeld et al.11 reported that enlarged adenoids are the leading cause of obstructive sleep apnea in children. This was also supported by various other studies.12, 13 and 14 Mora et al.15 in their study concluded that adenoidectomy played major role in the treatment of obstructive sleep apnea in children. Various other complications reported to have resulted from enlarged adenoids include failure to thrive, excessive daytime sleepiness, impairment of cognitive functions, poor school performance and psychosocial problems16, 17. Cardiac arrhythmia, left ventricular hypertrophy, heart failure, recurrent chest infection, breathlessness, pulmonary hypertension and cor-pulmonale have also been reported in the literature8, 18 and 19. These cardiorespiratory problems are due to the effect of hypoxia, endothelial dysfunction, oxidative stress and released inflammatory mediators20, 21, 22 and 23.
2
There have been extensive reports on children with enlarged adenoids and its effect on cardiorespiratory system from other part of the world12, 16and17. However there is a dearth of publications on enlarged adenoids and its effect on cardiorespiratory system in Nigeria. Fasunla et al24 found the prevalence of cardiac complication from enlarged adenoids to be 9.5% while
Dunmade et al10 reported respiratory infections in 50% of those with enlarged adenoids. This study therefore aims to add to the body of literature on the prevalence of cardiorespiratory complications among children with symptomatic enlarged adenoids and the pattern of cardiorespiratory and non cardiopulmonary complications in the affected children.
1.2 Epidemiology
Enlarged adenoids cause nasopharyngeal obstruction which in turn results in cardiorespiratory dysfunction8, 11. Published studies have shown prevalence of symptomatic enlarged adenoids to range between 0.7 – 4%25, 26, 27and28. The occurrence of adenoidal enlargement is thought to have gender equality but with earlier presentation in male29. However, few studies have recorded male preponderance of enlarged adenoids10, 30. Peak incidence occurs during preschool years30. Adenoidal enlargement is the leading cause of obstructive sleep apnea syndrome in children with the peak age of between 3 and 6 years11. Balbani et al. also showed that adenoidal hypertrophy in children has its peak incidence in pre - school age group24.
1.3 Justification for the study
Symptomatic adenoidal enlargement is a common condition for which children present at Ear, Nose and Throat clinic.31, 32and33. Its effect could impact negatively on the affected children’s growth and development
3
Its effects on cardiorespiratory system have been widely studied in other parts of the world however there are paucity of data on it in Nigeria. Early detection and treatment of these complications could lead to improvement in the cardiorespiratory outcomes22, 33and34. Few available studies that reported cardiorespiratory complications in Nigeria were on children with severe symptoms scheduled for surgery10, 24. This study, however, screened children with symptomatic enlarged adenoids for early detection of cardiorespiratory complications and will add to the body of literature on cardiopulmonary function of children with enlarged adenoids. Electrocardiography and x- ray are non invasive and easily applicable tools that can be used in evaluating affected children. Thus, this study aims to determine prevalence and pattern of cardiorespiratory complications among children with enlarged adenoids and any other associated non cardiopulmonary problems in children with enlarged adenoids attending Ear, Nose and Throat Clinic of Ladoke Akintola University of
Technology Teaching Hospital, Osogbo, Osun State, Nigeria.
4
CHAPTER 2
AIMS AND OBJECTIVES OF THE STUDY
General Objective
To evaluate the cardiorespiratory complications of enlarged adenoids among paediatric
patients at Ladoke Akintola University of Technology Teaching Hospital, Osogbo
Specific Objectives
To identify the various cardiorespiratory complications of enlarged adenoids in the paediatric
patients
To determine the prevalence of cardiorespiratory complications among patients with enlarged
adenoids
To identify other non-cardiopulmonary complications of enlarged adenoids in the patients
5
CHAPTER 3
LITERATURE REVIEW
Adenoid hypertrophy is one of the major causes of cardiorespiratory morbidities in children11, 15and18.
Enlarged adenoids with its attendant cardiorespiratory abnormalities in children has been implicated in the pathogenesis of obstructive sleep apnea, left ventricular dysfunction, right ventricular enlargement, right atrial enlargement, cardiac arrhythmia, congestive cardiac failure and pulmonary hypertension23, 35and36. Various studies have shown reversal of these cardiorespiratory complications following adenoidectomy5, 8and22.
3.1 PATHOGENESIS OF OBSTRUCTIVE SLEEP APNEA IN CHILDREN WITH
ENLARGED ADENOIDS
Enlarged adenoids predispose to paediatric obstructive sleep apnea syndrome and this has been shown by various studies 11, 12and15. Tal et al.8 reported that obstructive sleep apnea in children is almost always caused by enlarged adenoids and is cured by its removal. McCartney et al.18 reported three children with chronic obstructive sleep apnea and various cardiorespiratory complications that resulted from enlarged adenoids with resolution of the symptoms following adenoidectomy.
Enlarged adenoids narrow the airway with associated increased resistance30. Obstruction is worse during sleep and results in airflow dynamic changes in the upper airways which results in sleep apnea. Airway obstruction due to adenoidal hypertrophy may produce depressed arterial PaO2 and
37-42 elevated PaCO2 levels, which return to normal after adenoidectomy . Upper airway obstructive events are terminated by subcortical arousals induced by negative intrathoracic pressure, hypercapnoea and hypoxia which cause significant sleep disruption. Obstructive sleep apnoea may be associated with excessive daytime sleepiness due to interruptions of normal sleep with frequent
6 awakening during apnoeic episodes29. This can lead to neurobehavioral problems such as hyperactivity, irritability, bed- wetting and morning headache which can significantly affect a child’s quality of life42, 43and44.
3.2 PATHOGENESIS OF CARDIOVASCULAR DISEASE IN PATIENTS WITH
ENLARGED ADENOIDS
The pathogenesis of cardiovascular disease in children with enlarged adenoids has not been fully elucidated but various aetiologic mechanisms have been suggested. The cardiovascular system is disturbed by recurrent hypoxaemia, hypercapnoea, exaggerated intrathoracic pressure swing and arousal due to partial or complete airway obstruction by enlarged adenoids1,38 and multiple mechanisms proposed includes; increased sympathetic activities, inflammatory mediators in response to intermittent hypoxia and oxidative stress12, 38and39. Hypoxia and hypercapnoea lead to increase sympathetic activity by stimulating peripheral and central chemoreceptors. The sympathetic discharge causes vasoconstriction which raises peripheral resistance. The increased cardiac sympathetic stimulation results in tachycardia and a rise in blood pressure38, 41and45. The rise in pulmonary blood pressure as a result of increased sympathetic activity leads to transient pulmonary hypertension30 and if this is sustained will lead to right heart failure23, 30and 46. Study also showed that nocturnal hypoxaemia associated with partial or complete airway obstruction in enlarged adenoids influences incidence of atrial fibrillation, right heart failure and pulmonary hypertension16, 30and47.
Atrial fibrillation has been shown to be an important risk factor for heart failure and is associated with the degree of oxyhemoglobin desaturation. Patients with chronic airway obstruction have low plasma nitrite concentrations; this reduces bioavailability of endothelia derived nitric oxide and altered endothelial mediated vasodilatation48-53. Compromised endothelial mediated vasodilatation in the setting of increased sympathetic vasoconstrictor discharge would predispose patients with
7 obstructive adenoids to the development of hypertension54, 55and56. Hypoxia has also been shown to stimulate production of angiogenic substance like vascular endothelial growth factor (VEGF) 57, 58 and its concentration falls in response to reversal of obstruction58, 59and 60.
3.3 CARDIORESPIRATORY FINDINGS
Enlarged adenoids has clearly been demonstrated to be associated with the development of cardiorespiratory complications 16, 30 and studies have demonstrated various cardiorespiratory complications in patients with enlarged adenoids which resolved following adenoidectomy8, 18and 30.
These findings include; upper airway obstruction and obstructive sleep apnoea, reduced olfactory sensitivity, recurrent chest infections, cardiac arrhythmia, cardiomegaly, heart failure, left and right ventricular dysfunction and enlargement, pulmonary hypertension and cor- pulmonale23, 33and45.
Dumade et al.10 in their study reported that 87.5% of patients that had adenoidectomy were due to obstructive sleep apnea. Orji et al.63 reported respiratory problems in patients with adenoidal enlargement to include; snoring, mouth breathing, chronic nasal obstruction, obstructive sleep apnoea, and recurrent rhinorrhoea30. McCartney et al.18 reported three children with chronic obstructive sleep apnoea due to enlarged adenoids with resolution of the symptoms following adenoidectomy. Laurikainen et al.31 found 21% of 19 children aged 3 – 7 years with enlarged adenoids that developed left ventricular hypertrophy which resolved within six months of treatment with adenoidectomy. Mehmet et al.6 observed right and left ventricular dysfunctions in 29 patients with adenoidal hypertrophy which resolved following adenoidectomy and were not found in the control group. Gorur et al.28 found four out of thirty three patients with hypertrophic adenoids that developed right and left ventricular hypertrophy which resolved following adenoidectomy and were not present in age and sex marched control group. McCartney et al.18 also reported three cases with right atrial and ventricular hypertrophy, pulmonary hypertension, recurrent chest infection,
8 breathlessness, and heart failure due to obstructive adenoids which resolved following adenoidectomy.
3.4 RADIOLOGY OF ADENOID
Radiological imaging is complementary to the clinical evaluation of patients with enlarged adenoids.
Lateral plain radiograph of post nasal space was found to have relevance in establishing diagnosis and planning treatment in adenoidal enlargement61, 62. This will show relative size of adenoids to that of nasopharyngeal airway63, 64. Major et al.65 showed that lateral cephalographs performed reasonably well in evaluating adenoid size and that both quantitative measure of adenoid area and grading of its size on lateral cephalograms had reasonable correlation to adenoid size66, 67and68.
Adenoidal nasopharyngeal ratio (ANR) is usually calculated from lateral plain radiograph as the ratio of adenoidal depth to the nasopharyngeal depth.64 This is obtained by dividing distance from outermost point of convexity of adenoid shadow to basiocciput to the distance between sphenobasiocciput and posterior end of hard palate66, 69and70. (see the figure 3.45a below) ANR was first described by Fujioka in 1979 and later modified by Elwany in 198769, 70. ANR is an easily applicable, reliable and practical tool that can correctly measure the size of the adenoidal tissue in patients who are suspected to have adenoidal hypertrophy64, 66and 69. Kemaloghi et al.62 showed that
ANR is a more reliable method for determining whether adenoidal hyperplasia is clinically significant or not rather than the size of the adenoids or nasopharynx. Tezer et al.64 also showed that
ANR can give information about right ventricular functions in children with enlarged adenoids causing obstructive symptoms. Adenoidal nasopharyngeal ratio greater than 0.73 is indicative of pathological enlargement of the adenoids in children69,70. Magnetic resonance imaging and computerized tomographic scan (CT) of the nasopharynx are superior to plain radiograph in
9 assessing nasopharyngeal obstruction by adenoid tissue although they are expensive and are not routinely requested 9, 67.
Fig 3.4a
B P S
A B
B = Line drawn along straight part of anterior margin of basiocciput
S = Sphenobasioccipital synchondrosis
PS = Nasopharyngeal depth (line from anterior inferior edge of S to posterior superior margin of hard palate)
AB = Adenoid depth (perpendicular line from B to point of maximal convexity of Adenoid)
Adenoidal nasopharyngeal ratio (ANR) = Adenoid depth/ Nasopharyngeal depth (AB/AP).
10
3.5 ELECTROCARDIOGRAPHIC (ECG) FEATURES
Various ECG abnormalities in children with enlarged adenoids include; right atrial and ventricular hypertrophy left ventricular hypertrophy, deep T- wave inversion over right chest leads and peaked P waves.
Guror et al.4 reported four patients with right and left ventricular enlargement recorded from ECG with subsequent resolution following adenoidectomy. McCartney et al.18 reported three children with enlarged adenoids that developed severe cardiorespiratory problem with ECG abnormalities which include; right atrial and right ventricular hypertrophy, right ventricular strain, deep symmetrical T wave inversion over right ventricular leads, peaked P waves in lead II and R axis deviation. All these abnormalities resolved one to five months post adenoidectomy18.
3.6 OTHER IMPORTANT CAUSES OF CARDIOPULMONARY MORBIDITIES AND
MORTALITIES
Cardiopulmonary morbidity and mortality can be caused by other conditions that increase the risk of severe obstruction to the nasopharynx of children71. These include craniofacial disproportion and family predisposition71. Some craniofacial syndromes have coexisting airway hypotonia and hence greater tendency to obstructive breathing during sleep1. These conditions include; Crouzon syndrome, Treacher Collins syndrome, Apert syndrome and Beckwith- Wiedemann syndrome71.
Congenital cysts and masses like dermoid cyst, pharyngeal bursa (Thornwadt cyst), nasoalveolar cyst, meningocele, encephalocele, haemangioma, and teratoma can cause airway obstruction and cardiopulmonary problems71. Some systemic illnesses like Myotonic dystrophy, Cerebral palsy,
11
Obesity and glycogen storage disorder can also predispose to cardiorespiratory morbidities and mortalities1.
Inflammatory conditions which can be infective or allergic can cause rhinosinusitis in children with symptoms similar to those found in children with adenoid hypertrophy1. Children with allergic rhinosinusitis usually have negative skin prick tests for the first year or two of symptoms71. Affected children may also present with failure to thrive that is also seen in some children with adenoid hypertrophy71. Cow milk and egg proteins are the commonest responsible allergens. With increasing age these food sensitivities are usually lost and inhalant sensitivities gained 71.
Defect in complex system of defense mechanism which protects the lungs from hostile microbiological environment also predisposes affected individual to recurrent respiratory infections72. This system functions to prevent entry or to remove foreign materials from the lung.
Congenital lesions of the lung or heart can predispose affected individual to cardiorespiratory morbidities and mortalities72. Congenital defects like tracheo-oesophageal fistular, congenital heart disease, lobar sequestration, bronchial stenosis predispose to cardiorespiratory morbidities and mortalities. Congenital lesions are more common in syndromic children72.
One of the causes of cardiomegaly is cardiomyopathy. This usually predisposes affected children to congestive heart failure72. Cardiomyopathy is usually due to viral infection. Cardiomegaly can also be due to congenital heart disease, nutritional deficiency, chemotherapy and genetic disease72.
Inhaled foreign body’s especially organic foreign body like peanut evoked inflammatory reaction of the bronchial mucosa which leads to airway obstruction and infection71.
12
CHAPTER 4
METHODOLOGY
4.1 Study design
This was a prospective, cross sectional hospital based study conducted between July 2010 and June
2011. It involves children aged 8months – 12 years with clinical and radiographic diagnosis of enlarged adenoids.
4.2 Study location
Ear, Nose and Throat Department of Ladoke Akintola University of Technology Teaching Hospital,
Osogbo
4.3 SAMPLE SIZE DETERMINATION
The sample size for this study was calculated using the Leslie and Kish formula for sample size determination: 73
(N)= Z2 pq/d2
Where:
N = the desired sample size
Z= the standard normal deviation, usually set at 1.96 which corresponds to the 95 percent confidence level.
P=the proportion in the target population estimated to have particular characteristic. (Available prevalence of enlarged adenoid with symptoms of obstruction 4%)
13 q= 1.0-p. d= absolute deviation or amount of difference allowed between the target and the study population usually set at 0.05 (adjusted with error margin of 10%)
Hence, N = 1.962 x 0.04 x 0.96/ 0.052
N = 59.006976
Therefore, the estimated sample size is 60. However, a projected number of 90 was studied
4.4 Inclusion criteria
The inclusion criteria for the study were:
Patients age 8 months – 12 years
Patients with clinical and radiological evidence of adenoid enlargement
The clinical evidences that are suggestive of enlarged adenoids include mouth breathing,
snoring, nasal obstruction, nasal discharged, noisy breathing and obstructive breathing during
sleep. Other suggestive symptoms are recurrent ear infections and hearing impairment.
Radiologic evidence that is suggestive of adenoids is soft tissue mass at the nasopharynx that
narrows the airway.
Patients whose parent(s) gave informed consent to participate in the study
The control subjects were:
Age- and gender- matched children attending paediatric outpatient clinic for minor ailment.
Children with no clinical evidence suggestive of adenoid enlargement as stated above.
Children whose parent(s) gave informed consent to participate in the study.
14
4.5 Exclusion criteria for the study were:
Patients and control subjects with cleft palate
Patients and control subjects with previous history of adenoidectomy
Patients and control subjects whose parent(s) refused to give consent for participation in the
study.
4.6 PATIENTS AND METHODS
Informed consent was obtained from caregivers/parents of all eligible participants in the best understood language (English and Yoruba). I administered structured questionnaire to caregivers or parents of the patients for their demographic and clinical data. (See appendix 1)
Information/data obtained were:
(i) Identification no, age, sex
(ii) Detailed history of symptoms
(iii)General physical examination including thorough ear, nose and throat of the participants were
done.
(iv) The plain lateral radiographs of the nasopharynx of the affected children were obtained. The x –
ray film was taken by standard technique of lateral soft tissue radiograph of the nasopharynx.
The beam was centered to the external auditory meatus with the head in true lateral position
and the patient breathing through the nose with the mouth closed. The x - rays were reviewed
with a consultant Radiologist for the diagnosis of enlarged adenoids that caused significant
obstruction. The dimension of the adenoids and nasopharynx were measured with a
transparent rule using the standard landmarks designed by Fujioka (see appendix 3).
15
Adenoidal nasopharyngeal ratio was determined by dividing adenoidal depth with
nasopharyngeal depth. Chest radiograph were done in posterioanterior view (to avoid
apparent magnification of cardiac shadow associated with anterioposterior view). The patient
faces the film chin up with the shoulders rotated forward to displace the scapulae from the
lungs. The film was well collimated with centering point at T5 and a low KVP was used.
Chest radiographs were reviewed with consultant Radiologist. Radiographic evidence of
chest infection seen was mainly consolidative changes which range from patchy opacities to
homogeneous opacities. These opacities were either localized or diffused. Cardiomegaly was
determined using cardiothoracic ratio. This was calculated by using the maximum cardiac
diameter which was the horizontal distance of the most lateral aspect of the left and right
margin of the heart divided by the widest internal thoracic diameter. Cardiothoracic ratio of ≤
60 is usually used in infants as normal and value above this means cardiomegaly which was
used in this study.
(v) Electrocardiograph (ECG) was carried out on all the participants using ECG – 9803G. Standard
12 leads electrodes consist of limb (augmented) and chest electrodes. The body positions for
electrode attachment were cleaned with alcohol and gel was applied. Limb electrodes were
attached to right arm (RA), left arm (LA) and left leg (LL) while the neutral was attached to
right leg (RL). RA represents aVR, LA represents aVL and LL represents aVF. Between RA
and LA is lead I, between LA and LL is lead II and between LL and RA is lead III. The chest
electrodes were V1 (attached to forth intercostals space at right border of sternum), V2
(attached to forth intercostals space at left border of sternum), V3 (attached to midway
between V2 and V4), V4 (attached to fifth intercostals space at left mid-clavicular line), V5
(attached to left anterior axillary line at the horizontal level of V4) and V6 (attached to left
16
mid – axillary line at the horizontal level of V4). ECG results were reviewed with consultant
Cardiologist
4.7 Data analysis
Data were collated and presented in descriptive format, tables, diagrams and graphs where appropriate. Continuous and categorical variables were displayed as mean ± standard daviation (SD) and percentage respectively. Differences between categorical variables were analysed by Chi-square test. Student’s t- test was used to assess differences between continuous variables. Differences between three or more continuous variables were analysed using analysis of variance (ANOVA) test.
The relationships between adenoidal nasopharyngeal ratio and age, gender, ECG findings, duration of illness and chest infections were also assessed. The level of significance was put at < 0.05. All analysis was done using Statistical Package for Social Sciences (SPSS) version 14.0 (SPSS Inc,
Chicago, IL, USA).
17
4.8 ETHICAL CONSIDERATION
Ethical clearance for this study was obtained from the Research Ethics Committee of Ladoke
Akintola University of Technology Teaching Hospital, Osogbo.
18
CHAPTER 5
RESULTS
Participants included 90 subjects and 90 controls. The age ranged between 8 months and 12 years.
The mean age + SD subjects: controls = 2.42 + 1.03: 2.71 + 0.77 years. Among the subjects, males: females were 61: 29 while among the controls males: females were 58: 32. Male: female ratio of
2.1:1 (subjects) and 1.8: 1 (controls). The largest proportions were in age group (12 to 71) months in both the subjects and the controls while the least proportions were in age group (72 to 144) months among the subjects and the controls.
TABLE 1: AGE DISTRIBUTION OF SUBJECTS AND CONTROLS
Age range (months) Subjects (%) Controls (%)
8 – 11 17 (18.9) 1 (1.1)
12 – 35 33 (36.7) 38 (42.2)
36 – 71 29 (32.2) 39 (43.3)
72 – 107 7 (7.8) 10 (11.1)
108 – 144 4 (4.4) 2 (2.2)
Total 90 (100) 90 (100)
Table 1 showed the age distribution of the subjects and the controls.
19
TABLE 2: GENDER DISTRIBUTION OF SUBJECTS AND CONTROLS
SUBJECTS CONTROLS
GENDER N = 90 (%) N= 90 (%)
MALE 61 (67.8) 58 (64.4)
FEMALE 29 (32.2) 32 (35.6)
TOTAL 90 (100) 90 (100)
Table 2 showed gender distribution of the study population.
20
FIG 1: BAR CHART SHOWING AGE PREVALENCE AMONG THE SUBJECTS AND
THE CONTROLS (N=90)
21
TABLE 3: DISTRIBUTION OF SYMPTOMS AND SIGNS OF ADENOID ENLARGEMENT
(n = 90)
Symptoms No of patients Percentage (%)
Snoring 88 97.8
Nasal obstruction 90 100
Nasal discharge 87 96.7
obstructive breathing during sleep 74 82.2
Mouth breathing 89 98.9
Excessive daytime sleepiness 15 16.7
Otorrhoea 6 6.7
Hearing loss 2 2.2
Table 3 showed the distribution of symptoms among the subjects. Recurrent nasal obstruction was the most common symptom occurring in 100% of the subjects whilst hearing loss was the least common symptom occurring in 2.2% of the subjects.
22
FIG 2: PIE CHART SHOWING OTHER ABNORMAL FINDINGS IN SUBJECTS
WITH ADENOID ENLARGEMENT
Other findings among subjects with adenoids included failure to thrive in 10(11.1%) and chest wall deformity 4(4.4%).
23
The adenoidal nasopharyngeal ratio (ANR) of subjects ranges from 0.60 – 0.89. This was further grouped into mild obstruction (0.60 – 0.69), moderate obstruction (0.70 – 0.79) and severe obstruction (0.80 – 0.89).
TABLE 4: DISTRIBUTION OF ADENOIDAL NASOPHARYNGEAL RATIO OF THE SUBJECTS
Adenoidal Nasopharyngeal Frequency Percentage (%) Ratio
0.60 – 0.69 11 12.2
0.70 – 0.79 21 23.3
0.80 – 0.89 58 64.4
Total 90 100
Table 4 showed the distribution of adenoidal nasopharyngeal ratio among the subjects. Severe obstruction was the predominant group (64.4%) while mild obstruction was the least (12.2%).
24
TABLE 5: ASSOCIATION BETWEEN ADENOIDAL NASOPHARYNGEAL RATIO AND AGE GROUP (MONTHS)
Adenoidal Nasopharyngeal Ratio 0.60- 0.69 0.70- 0.79 0.80-0.89 Total Age groups in months N= 11 (%) N= 21 (%) N= 58 (%) N= 90 (%)
8 – 11 1 (9.1) 3 (14.3) 13 (22.4) 17 (18.9)
12 – 35 4 (36.4) 7 (33.3) 22 (37.9) 33 (36.7)
36 – 71 4 (36.4) 6 (28.6) 19 (32.8) 29 (32.2)
72 – 107 0 (0.0) 3 (14.3) 4 (6.9) 7 (7.8)
108 – 144 2 (18.1) 2 (9.5) 0 (0.0) 4 (4.4)
Total 11 (12.2) 21 (23.3) 58 (64.5) 90 (100)
X2 = 11.94; P = 0.03
Table 5 showed association between adenoidal nasopharyngeal ratio and age of the subjects. Age group (12 to 35) months had greatest degree of nasopharyngeal obstruction while age group (108 to 144) months had least degree of nasopharyngeal obstruction. There was significant association between age and degree of nasopharyngeal obstruction by adenoid tissue (X2 = 11.94; P < 0.05).
25
TABLE 6: ASSOCIATION BETWEEN ADENOIDAL NASOPHARYNGEAL RATIO AND SEX
Adenoidal nasopharyngeal Sex of Subjects Total Ratio Male Female N= 90 (%) N= 61 (%) N= 29 (%) 0.60 – 0.69 6 (9.8) 5 (17.2) 11 (12.2)
0.70 – 0.79 15 (24.6) 6 (20.7) 21 (23.4)
0.80 – 089 40 (65.6) 18 (62.1) 58 (64.4)
Total 61 (67.8) 29 (32.2) 90 (100)
X2 = 1.05; P = 0.70.
Table 6 showed association between adenoidal nasopharyngeal ratio and sex among the subjects.
There was no significant association between them P > 0.05
26
TABLE 7: ELECTROCARDIOGRAPHIC (ECG) FINDINGS AMONG THE SUBJECTS
AND THE CONTROLS
ECG FINDINGS SUBJECTS (%) CONTROLS (%)
NORMAL 75 (83.3) 89 (98.9)
ABNORMAL 15 (16.7) 1 (1.1)
TOTAL 90 (100) 90 (100)
Table 7 showed electrocardiographic (ECG) findings among the subjects and the controls.
Among the subjects 16.7% had abnormal ECG findings while only 1.1% of the controls had abnormal ECG findings.
27
TABLE 8: PATTERN OF ELECTROCARDIOGRAPHIC (ECG) ABNORMALITY
AMONG THE SUBJECTS AND THE CONTROLS
ECG FINDINGS SUBJECTS (%) CONTROLS (%)
NORMAL 75 (83.3) 89 (98.9)
RVH 5 (5.6) 1 (1.1)
LVH 9 (10.0) -
BVH + LAE 1 (1.1) -
TOTAL 90 (100) 90 (100)
Table 8 showed pattern of ECG abnormality among the subjects. Left ventricular hypertrophy was the predominant abnormal finding (10%) while biventricular hypertrophy with left atrial enlargement was the least abnormal finding (1.1%).
28
TABLE 9: PREVALENCE OF CHEST INFECTION AMONG THE SUBJECTS
AND THE CONTROLS
CXR Findings Subjects (%) Controls (%)
Normal 68 (75.6) 83 (92.2)
Chest infection 22 (24.4) 7 (7.8)
Total 90 (100) 90 (100)
Table 9 showed that 22 (24.4%) of subjects had chest infections while only 7(7.8%) of control group had chest infections. Chest radiograph also showed cardiomegaly in 6 subjects which was not present in the control group.
29
TABLE 10: ASSOCIATION BETWEEN ECG FINDINGS AND ADENOIDAL
NASOPHARYNGEAL RATIO
ECG Findings
Adenoidal nasopharyngeal ratio Normal Abnormal Total
N= 75 (%) N= 15 (%) N= 90 (%)
0.60 – 0.69 11(14.7) 0 (0) 11 (12.2)
0.70 – 0.79 20 (26.7) 1 (6.7) 21 (23.3)
0.80 – 0.89 44 (58.7) 14 (93.3) 58 (64.5)
Total 75 (83.3) 15 (16.7) 90 (100)
X2 = 6.67; P = 0.04
Table 10 showed that the greater the severity of obstruction of the nasopharynx by the adenoid tissue the higher the tendency to develop abnormal ECG (P < 0.05).
30
TABLE 11: ASSOCIATION BETWEEN ECG FINDINGS AND AGE OF THE
SUBJECTS
AGE GROUP (months) ECG findings Total
Normal Abnormal N= 90 (%)
N=75 (%) N=15 (%)
8 – 11 12 (16) 5 (33.3) 17 (18.9)
12 – 35 28 (37.3) 5 (33.3) 33 (36.7)
36 – 71 26 (34.7) 3 (20) 29 (32.2)
72 – 107 6 (8) 1 (6.7) 7 (7.8)
108 – 144 3 (4) 1 (6.7) 4 (4.4)
Total 75 (83.3) 15 (16.7) 90 (100)
X2 = 3.11; P = 0.40
Table 11 showed that abnormal ECG was more common in younger age group (8 to 35) months compared with older age group (72 – 144) months (66.7% vs. 13.3%, p = 0.40).
31
TABLE 12: ASSOCIATION BETWEEN SEX AND ECG FINDINGS AMONG THE
SUBJECTS
SEX OF PATIENTS
ECG FINDINGS TOTAL Male Female N=90 (%) N= 61 (%) N= 29 (%)
Normal 48 (78.7) 27 (93.1) 75 (83.3)
Abnormal 13 (21.3) 2 (6.90) 15 (16.7)
Total 61 (67.8) 29 (32.2) 90 (100)
X2 = 2.98; P = 0.09
Table 12 showed that abnormal ECG findings was more common in the males compared with the females (21.3% vs. 6.9 %, p = 0.09).
32
TABLE 13: ASSOCIATION BETWEEN ECG FINDINGS AND DURATION OF
ILLNESS AMONG THE SUBJECTS
ECG findings
Duration (Months) Total Normal Abnormal N= 90 (%) N=75 (%) N= 15 (%)
0 – 6 27 (36) 3 (20) 30 (33.3)
7 – 12 22 (29.3) 8 (53.4) 30 (33.3)
13 – 24 14 (18.7) 2 (13.3) 16 (17.8)
>24 12 (16) 2 (13.3) 14 (15.6)
Total 75 (83.3) 15 (16.7) 90 (100)
X2 = 3.38; P = 0.86
Table 13 showed that duration of illness was not significantly associated with ECG abnormality
(p > 0.05).
33
TABLE 14: ASSOCIATION BETWEEN CHEST INFECTION AND ADENOIDAL NASOPHARYNGEAL RATIO AMONG THE SUBJECTS
Chest findings Adenoidal nasopharyngeal ratio Total Normal Chest infection N = 90 (%) N= 68 (%) N= 22 (%)
0.60 – 0.69 10 (14.7) 1 (4.6) 11 (12.2)
0.70 – 0.79 18 (26.5) 3 (13.6) 21 (23.3)
0.80 – 0.89 40 (58.8) 18 (81.8) 58 (64.5)
Total 68 (75.6) 22 (24.4) 90 (100)
X2 = 3.94; P < 0.05
Table 14 showed that chest infection was more common in children with largest ratio of ANR compared with those with the least ratio of ANR (81% vs. 4.6%, p < 0.05).
34
TABLE 15: ASSOCIATION BETWEEN CHEST INFECTION AND AGE OF THE
SUBJECTS
CXR findings
Age groups (months) Normal Chest infection Total
N = 68 (%) N = 22 (%) N = 90 (%)
8 – 11 13 (19.1) 4 (18.2) 17 (18.9)
12 – 35 27 (39.7) 6 (27.3) 33 (36.7)
36 – 71 19 (27.9) 10 (45.4) 29 (32.2)
72 – 107 5 (7.4) 2 (9.1) 7 (7.8)
108 -144 4 (5.9) 0 (0) 4 (4.4)
Total 71 (78.9) 19 (21.1) 90 (100)
X2 = 2.2; P = 0.46.
Table 15 showed that chest infection was more common in the younger age group (8 – 71) months compared with the older age group (72 – 144) months (90.9% vs. 9.1%, p = 0.46).
35
TABLE 16: ASSOCIATION BETWEEN CARDIOMEGALY AND ADENOIDAL
NASOPHARYNGEAL RATIO
CXR findings
Adenoidal nasopharyngeal Normal Cardiomegaly Total
ratio N = 84 (%) N = 6 (%) N = 90 (%)
0.60 – 0.69 11 (13.1) 0 (0) 11 (12.2)
0.70 – 0.79 21 (25) 0 (0) 21 (23.3)
0.80 – 0.89 52 (61.9) 6 (100) 58 (64.5)
Total 84 (93.3) 6 (6.7) 90 (100)
X2 = 67.6; P < 0.001
Table 16 showed that cardiomegaly was predominantly found in patients with severe obstruction of the nasopharynx by the adenoid tissues.
36
CHAPTER 6
DISCUSSION
The prevalence of cardiac complication from adenoid enlargement in this study was 16.7% among the subjects and 1.1% among the controls. Other studies have reported cardiac complication from enlarged adenoid to range between 9.5 – 61.1%4, 6, 24and33. Laurikainen et al.33 in Finland reported prevalence of cardiac complication from adenoid enlargement of 21%, Fasunla et al.24 in Ibadan,
Nigeria reported a prevalence of 9.5%. However, Tal et al.6 in Israel reported a prevalence of 61%.
The higher prevalence in Tal study was due to the fact that radionuclide scanning was used to assess the cardiovascular status of the affected children which is more sensitive in evaluation of heart functions.
Cardiac abnormalities observed from this study include left ventricular hypertrophy which occurred in 10% of the subjects, right ventricular hypertrophy 5.5%, and biventricular hypertrophy with left atrial enlargement 1.1%. The only abnormal finding among the control was right ventricular hypertrophy which occurred in only 1.1%. Gorur et al.4 reported left and right ventricular dysfunctions in children with enlarged adenoids and were not found in the control group.
McCartney et al.18 reported cor pulmonale in three children who had obstructive adenoids with electrocardiographic diagnosis of right atrial enlargement, right ventricular hypertrophy and right axis deviation. Fasunla et al.24 in Nigeria observed that 4% of the children in their study had right ventricular hypertrophy which was similar to the findings from this present study, though their study did not find isolated left ventricular hypertrophy. Other cardiac abnormalities from their study included bi-ventricular hypertrophy, right atrial enlargement and right axis deviation. The reason for the preponderance of left ventricular hypertrophy in this study was, however, not known and further study in this area is therefore suggested. Most of these reported abnormalities (RVH, LVH,
37
RAE and LAE) resolved following adenoidectomy33, 76. However, adenoidectomy has not been done for the affected children in this study to further evaluate their cardiovascular status.
Six patients (6.7%) had cardiomegaly which was not present in the control group. All the subjects with cardiomegaly had severe nasopharyngeal obstruction. This was similar to the findings by
Gorur et al.4 who documented that 2 out of the 33 (6%) children with enlarged adenoids had cardiomegaly. However, McCartney et al.18 reported cardiomegaly among all the three cases he reported with subsequent resolution after adenoidectomy. The degree of nasopharyngeal airway obstruction by adenoids appears to predispose these patients to the development of abnormal cardiac function as there was significant association between degrees of nasopharyngeal obstruction and abnormal ECG recorded p = 0.01. (Table 10)
The prevalence of chest infection from this study was 24.4%. Dumade et al.10 in Ilorin reported the prevalence of chest infection among 28 children scheduled for adenoidectomy of 50% (though his study was not a controlled study). McCartney et al.18 found recurrent chest infection in all the three cases they reported. The prevalence of chest infection in this present study was highest among patients with greatest adenoidal nasopharyngeal ratio (94.7%) (Table 14), consistent with other reports10, 18. Chest infection was also common among age groups 1 to 6 years. This was the age where greater proportion of subjects had largest adenoidal nasopharyngeal ratio. This subsequently predisposes their airway to colonization by microorganisms and hence greater chance of developing respiratory infections. This age bracket corresponds to the time interval children start developing their immune status with lesser tendency to fight or resist microorganisms.
The prevalence of failure to thrive in this study was 11.1%, this was higher than 6.7% reported by
Fasunla et al.24 but was much lower than 50% reported by Dunmade et al.10 The higher prevalence reported by Dunmade et al may be due to the smaller study population. Abnormal ECG findings
38 were found in 40% of patients with failure to thrive. This association was however not reported by previous studies. Enlarged adenoids may predispose to growth and cardiorespiratory failure13.
Cardiorespiratory failure predisposes to chronic hypoxia as well as poor feeding habits1, 76 and subsequent failure to thrive. Impairment of growth hormone function seen in children with enlarged adenoids also predisposes affected children to failure to thrive1.
Clinical symptoms of enlarged Adenoids
The most prevalent symptoms in this study were snoring, chronic nasal obstruction, recurrent mucopurulent nasal discharge, obstructive breathing during sleep and mouth breathing. The symptomatology of obstructive adenoids reported in this series was similar to the findings in previous similar studies10, 76and77. These symptoms have been linked with obstructive adenoids in children, though other rhinologic conditions in children could present with similar symptoms24.
Orji et al.65 in Enugu reported that clinical rating of adenoidal symptoms (snoring, mouth breathing and obstructive breathing during sleep) in children provide reasonably reliable assessment of the presence and severity of nasopharyngeal airway obstruction by adenoid tissue. Dumade et al.10 in Ilorin reported that adenoid enlargement was responsible for 87.5% of cases of obstructive sleep apnoea in their study. Paradise et al.68 reported that the presence of mouth breathing provide reliable and reasonably valid assessment of the degree of adenoidal obstruction of the nasopharyngeal airway. Bitar et al.77 devised a clinical score for identifying children that will require adenoidectomy. These symptoms included mouth breathing, snoring obstructive breathing during sleep, restless sleep and frequent wake up at night.
The prevalence of excessive daytime sleepiness was 16.7%. This was higher than 10.8% reported by Fasunla et al.24 Excessive daytime sleepiness may lead to poor school performance and
39 psychosocial problems with its negative impact on the quality of life of the affected children and their family.
Sex distribution showed significant male preponderance of 67.8% and male to female ratio of 2.1:
1.0. This was similar to the findings from other studies 10, 65, 76where male preponderance ranged between 60.5 – 75.0 percent. The reason for the male preponderance is however not known.
Age distribution showed that the peak prevalence of adenoid enlargement occurred in the age group
12 to 35 months while the least age group was 108 to 144 months. This is consistent with findings from previous studies10, 24and65. The explanation for this finding is that adenoids grow more rapidly than the bony structure of the nasopharynx in this age group with consequent decrease in the size of nasopharyngeal airway3, 4and5. This trend reverses from age 7 years and above when adenoids starts to regress while nasopharynx continues to grow74, 76. Hence, clinical symptoms are more common in the younger age group due to relative small volume of the nasopharynx3, 4and5. Other factor responsible for this is the increase frequency of upper respiratory infections in younger children which was shown to cause adenoid enlargement and ultimately leads to nasopharyngeal airway obstruction1. The consequence of these factors is a relatively smaller nasopharyngeal airway in younger children. The children in this age group therefore present more frequently with obstructive adenoidal symptoms.
Adenoids and Nasopharyngeal Airway
In this study, severe obstruction was observed in large proportion of subjects (64.4%). Higher prevalence of severe obstruction (54.8%) was reported by Orji et al.65 However, Fasunla et al.24 reported 31.1% prevalence of severe obstruction in their study. There was significant association between age and the degree of nasopharyngeal obstruction by adenoids p < 0.05 (Table 5). The degree of nasopharyngeal obstruction was most severe in the age group 12 to 35 months. This was
40 similar to the findings by Bitar et al.77 and consistent with findings from other studies10, 32and65.
There was significant association between adenoidal nasopharyngeal ratio and abnormal electrocardiographic findings as shown by this study p = 0.01 (Table 11). Fasunla et al.24 reported similar findings. They also reported resolution of cardiac complications in two children, persistence of the abnormal cardiac findings in three children within five months of adenoidectomy while two children were lost to follow up. However, in this present study, most of the affected children were yet to be operated on to allow for their post operative re-evaluation.
This study also revealed significant association between chest infection and adenoidal nasopharyngeal ratio (p < 0.01). There was higher proportion of male with greater degree of nasopharyngeal obstruction than female but this was however not statistically significant (p > 0.05).
Kemaloghi et al.64 showed that adenoidal nasopharyngeal ratio is more reliable than the size of adenoids at determining the significant adenoidal hyperplasia. Tezer et at.66 reported that adenoidal nasopharyngeal ratio can give information about right ventricular functions in children with enlarged adenoids. Hence, adenoidal nasopharyngeal ratio as shown from this study and supported by other previous studies is a useful tool that can be employed to determine whether adenoidal hypertrophy is clinically significant or not. It can also be used to predict any child that might develop cardiorespiratory complications from enlarged adenoids.
41
CONCLUSION
Adenoidal nasopharyngeal ratio was found to be a useful tool in assessing cardiorespiratory complications in children with enlarged adenoids.
Electrocardiograph (ECG) was found to be useful in diagnosing various cardiac anomalies associated with adenoidal enlargement and chest radiograph was useful at detecting chest infection which is prevalent in these patients.
Physical evaluation revealed other non cardiorespiratory complications in children with enlarged adenoids, therefore affected children should have thorough physical examination.
.
42
RECOMMENDATIONS
Symptoms of snoring, recurrent nasal discharge, mouth breathing, nasal obstruction and obstructive breathing during sleep were found in this study and prevalent in patients with adenoid enlargement.
A scoring system of these symptoms (see appendix 6) is recommended and should be made available to community health officers and other related health workers that serve as first point of contact for the patients for early and prompt referral.
Adenoidal nasopharyngeal ratio is recommended to be used by Otorhinolaryngologist for determining children with clinical significance of adenoid enlargement as well as those that may need surgical intervention
All patients with adenoid enlargement should be referred for thorough Otorhinolaryngological evaluation.
43
BENEFIT OF THE STUDY TO PARTICIPANTS, SCIENCE & KNOWLEDGE
1. The outcome of this study has helped in making appropriate recommendations for the patients,
caregivers and community at large. This will help to prevent associated problems with adenoid and
improve patients’ quality of life.
2. Outcome has added to the available body of knowledge in our environment on the effect of enlarged
adenoid on cardiorespiratory system of children.
LIMITATIONS
1. The patients and controls were not assessed using echocardiography which is more sensitive than
ECG in the assessment of LAE, RAE, LVH and RVH.
2. X - ray post nasal space assessment of the controls were not done to reduce risk of excessive
irradiation.
44
REFERENCES
1. Peter JR. The adenoid and adenoidectomy. In Scott- Brown’s Otolaryngology, Vol. 1: 7th
edition, (Michael G, George GB, Martin JB, et al. eds), Hodder Arnold London. 2008; 1095-
1101.
2. Jaw TS, Sheu RS, Liu GC, Lin WC. Development of adenoids: a study by measurement with
MRI images. Kaossiung J Med Sci 1999; 15: 12-18.
3. Nixon GM, Brouillette RT. Sleep. 8: Paediatric obstructive sleep apnea. Thorax 2005; 60:
511- 516.
4. Gorur K, Doven O, Unal M, Akkus N, Ozcan C. Preoperative and Post operative cardiac and
clinical findings of patients with adenotonsillar hypertrophy. Int J Paediatric
Otorhinolaryngol 2005; 59 (1): 41- 46.
5. Mehmet BU, Sait MD, Ayhan S, Ayhan S, Lokman U, Fikret C et al. Effect of adenoidectomy /
Tonsillectomy on cardiac functions in children with obstructive sleep apnoea.
Otorhinolaryngo10, 32, 65 l. 2008; 70 (3): 2002- 2008.
6. Hata M, Asakura K, Saito H. Profile of Immunoglobulin production in adenoid and tonsil
lymphocytes. Acta Otolaryngol Suppl. 1996; 523: 84 – 86.
7. Tal A, Leiberman G, Marguils G, Sofer S. Ventricular dysfunction in children with
obstructive sleep apnea: radionuclide assessment. Paediatric Pulmonol. 1988; 4 (3): 139- 143.
8. Potsic WP, Pasquariello PS, Baranak CC, Marsh RR, Miller LM. Relief of upper airway
obstruction by adenotonsillectomy. Otolaryngol Head Neck Surg. 1986; 94(4): 476- 480.
9. Arens R, McDonough JM, Costarino AT, Mahboubi XE, Tayag-Kier CE, Maislin G et al.
Magnetic resonance imaging of the upper airway structure of children with obstructive sleep
apnea syndrome. Am J Respir Crit Care Med. 2001; 164(4): 698- 703.
45
10. Dunmade AD, Alabi BS. Daycase adenoidectomy: Is it safe? Niger J Clin Pract 2009; 12
(12): 45- 48.
11. Greenfeld M, Tauman R, DeRowe A, Sivan Y. Obstructive sleep apnea syndrome due to
adenotonsillar hypertrophy in infants. Int J Paediatr Otolaryngol. 2003; 67(10): 1056- 1060.
12. Schulz R, Grebe M, Eisele HJ, Mayer K, Weissmann N, Seeger W. Obstructive sleep apnea-
related cardiovascular disease. Med Klin 2006; 101(4): 321- 327.
13. Chopo GR, Lazaro MA, Ucles P. Obstructive sleep apnea syndrome in childhood. Rev.
Neurol. 2001; 32(1): 86- 91.
14. Villa AJR, de Mignel DJ. Obstructive sleep apnea syndrome in childhood. An Esp Paediatr.
2001; 54(1): 58- 64.
15. Mora R, Salami A, Passali FM. Obstructive sleep apnea syndrome in children. Int J Paediatr
Otolaryngol.2003; 67 suppl 1: S229-231.
16. Jason MG, Virend KS, Sean MC. Obstructive Sleep Apnea, Cardiovascular Disease and
Pulmonary Hypertension. The Proceedings of the American Thoracic Society 2008; 5: 200-
206.
17. Hiren M, Raanas A. Diagnosis issues in Paediatric Obstructive sleep Apnea. The Proceedings
of the American Thoracic Society 2008; 5: 263- 273.
18. Macartney FJ, Panday J, Scott O. Cor Pulmonale as a result of chronic nasopharyngeal
obstruction due to hypertrophied tonsils and adenoids. Arch Dis Child 1969; 44: 585- 592.
19. Xhifei XU, Daniel KLC, So LL. Clinical Evaluation in Predicting Childhood Obstructive
Sleep Apnea. Chest 2006; 130(6): 1765- 1771.
46
20. Khayat R, Patt B, Hayes DJ. Obstructive sleep apnea: the new cardiovascular disease. Part 1:
Obstructive sleep apnea and the pathogenesis of vascular disease. Heart fail Rev. 2009;
14(3): 143- 153.
21. Thanopoulos B, Ikkos DD, Milingos M, Foutakis D. Cardiorespiratory syndrome due to
enlarged Tonsil and adenoids. Acta Paediatrica 2008; 64(4): 659- 663.
22. Raphael S, Joseph F, Arthur IE. Obstructive hypertrophic adenoids and tonsils as a cause of
infantile failure to thrive: Reversed by tonsillectomy and adenoidectomy. Int J Paediatr
Otolaryngol. 1985; 9(2): 183- 187.
23. Glen GC, Ernest EJ, Bernard EL et al. Heart Failure Due to Enlarged Tonsils and adenoids.
Am J Dis Child. 1969; 118(5): 708 - 717.
24. Fasunla AJ, Onakoya PA, Ogunkunle OO, Mbam TT, Nwaorgu OGB. Routine
Electrocardiography Request in Adenoidectomy: Is it necessary? Indian J Otolaryngol Haed
Neck Surg. 2011; DOI 10.1007/s12070-011-0264-0
25. Sogut A, Altin R, Uzun L, Ugur MB, Tomac N, Acun C et al. Prevalence of obstructive sleep
apnea syndrome and associated symptoms in 3- 11 yrs old Turkish children. Paediatric
Pulmonol. 2005; 39(3): 251- 256.
26. Aetna. Obstructive sleep Apnea in Children. Clinical Policy Bulletin: 2010; No: 0752.
27. Al – Ghamdi SA, Manoukian JJ, Morielli A, Kamaldine O,Ducharme FM, Brouillette RT. Do
Systemic Corticosteroids Effectively Treat Obstructive Sleep Apnea Secondary to
Adenotonsillar Hypertrophy? The Laryngoscope 2009; 107(10): 1382- 1387.
28. Cioffi G, Russo TE, Stefenelli C, Selmi A, Furlanello F, Cramariuc D et al. Severe
obstructive sleep apnea elicits concentric left ventricular geometry. J Hypertens. 2010; 28(5):
1074-1082.
47
29. Helen MC. Obstructive sleep apnea in childhood. In Scott- Brown’s Otolaryngology, Vol. 1:
7th edition, (Michael G, George GB, Martin JB, et al. eds), Hodder Arnold London. 2008;
1102- 1113.
30. Orji FT, Okolugbo NE, Ezeanolue BC. The role of adenoidal obstruction in the pathogenesis
of otitis media with effusion in Nigeria Children. Niger J Med. 2010 ;19(1):62-68
31. Laurikainen E, Aitasalo K, Erkinjuntti M, Wanne O. Sleep apnea syndrome in children- -
secondary to adenotonsillar hypertrophy. Acta Otolaryngol 1992; 492: 38- 41.
32. Dunai A, Mucsi I, Juhasz J, Novak M. Obstructive sleep apnea and cardiovascular disease.
Orv Hetil 2006; 47(48): 2303-2311.
33. Subashini P, Ravikumar A, Ranjit MS et al. Adenoid hypertrophy presenting with systemic
hypertension. Ind J Otolaryngol Head and Neck Surg 2007; 59(1): 73-75.
34. Kenny PP, Abhilash B. Paediatric obstructive sleep apnoea: Is polysomnography always
necessary? J Laryngol Otol 2004; 118(4): 275-278.
35. Dai Y, Baradley TD. Pathogenesis of atherosclerosis- Is Obstructive sleep apnea a new kid
on the block? Am J Respir Crit Care Med. 2007; 176: 634- 635.
36. Schluter B, Buschatz D, Trowitzsch E, Andler W. Sleep apnea in hyperplasia of the
pharyngeal lymphatic tissue. Polysomnographic studies in children. Monatsschr Kinderhei
lkd. 1993; 141(2): 124-129.
37. Khalifa MS, Kamei RH, Zikry MA, Kandil TM. Effect of enlarged adenoids on arterial blood
gases in children. J Laryngol Otol 1991; 105: 436 – 438.
38. Narkiewick K, Montano N, Cogliati C. Altered Cardiovascular Variability in Obstructive
Sleep Apnea. Circulation 1998; 98(11): 1071- 1077
48
39. Virend K, Mark ED, Mary PC, Francois MA. Sympathetic Neural Mechanisms in
Obstructive sleep apnea. J Clin Invest. 1995; 96: 1897- 1904.
40. Morgan BJ, Denahan T, Ebert TJ. Neurocirculatory Consequences of negative intrathoracic
pressure vs. asphyxia during voluntary apnea. J Appl Physiol. 1993; 74: 2969- 2975.
41. Somers VK, Mark AL, Zavala DC. Contrasting effect of hypoxia and hypercapnia on
ventilation and sympathetic activity in human. J Appl Physiol. 1989; 67: 2101- 2106.
42. Bradley TD, John SF. Sleep apnea and Heart Failure – Part I: Obstructive Sleep apnea.
Circulation 2003; 107: 1671-1678.
43. Guilleminault C, Palayo R, Ledger D, Bocian RC. Recognition of sleep disordered breathing
in children. Paediatrics. 1996; 98: 871- 882.
44. Sonn H, Rosenfield RM. Evaluation of sleep disordered breathing in children. Otolaryngol H
N Surg. 2003; 128: 344- 352.
45. Sie KN, Perkins JA, Clarke WR. Acute right heart failure due to adenotonsillar hypertrophy.
Int J Paed Otolaryngol. 1997; 41: 53- 58.
46. Geiser T, Buck F, Meyer BJ. In vivo platelets activation is increasing during sleep in
patients with obstructive sleep apnea syndrome. Respiration 2002; 69: 229- 234.
47. Von KR, Dimsdale J. Hemostat alterations in patients with obstructive sleep apnea and
implication s for cardiovascular disease. Chest 2003; 124: 1956-19 67.
48. Nobili L, Schiavi G, Bozano E et al. Morning increase of whole blood viscosity in
obstructive sleep apnea syndrome. Clin Hemorheol Micro Circ 2002; 2: 21- 27.
49. Chin K, Ohi M, Kila H et al. Effects of NCPAP therapy of fibrinogen levels in obstructive
sleep apnea syndrome. Am J Respir Crit Care Med 1996; 153: 1972- 1976.
49
50. Hui DS, Ko FD, Fok JP et al. The Effect of nasal CPAP or platelets activation in obstructive
sleep apnea syndrome. Chest 2004; 125: 1768- 1775.
51. Shamsuzzaman AS, Winnicki M, Lanfranchi P Elevated C- reactive protein in patients with
obstructive sleep apnea. Circulation 2002; 105: 2462- 2464.
52. Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecule expression and production
of reactive oxygen species in leukocytes of sleep apnea patients. Am J Respir Crit Care Med.
2002; 165: 939- 943.
53. Ip MS, Lam B, Chan LY. Circulating nitric oxide is suppressed in obstructive sleep apnea
and is reversed by nasal CPAP. Am J Crit Care Med. 2000; 162: 2166- 2171.
54. Peppard PE, Young T, Palta M. Prospective study of the association between sleep
disordered breathing and hypertension. N Eng J Med. 2000; 342: 1378- 1384.
55. Somer VK, Dyken ME, Clary MP, Abboudn FM et al. Sympathetic neural mechanisms in
obstructive sleep apnea. J Clin Invest. 1995; 96: 1897- 1904.
56. Canson JT, Rangemark C, Hedner JA. Attenuated endothelium- dependent vascular
relaxation in patients with sleep apnea. J Hypertens. 1996; 14: 577- 584.
57. Fletcher EC, Lesske J, Cuman J. Sympathetic denervation blocks blood pressure elevation in
episodic hypoxia. Hypertension. 1992; 20: 612- 619.
58. Schultz A, Lavie L, Hochberg I. Interindividual heterogeneity in the hypoxic regulation of
VEGF: Significance for the development of the coronary artery collateral circulation.
Circulation 1999; 100: 547- 552.
59. Schulz R, Hummel C, Heinemann S. Serum levels of vascular endothelial growth factor is
elevated in patients with obstructive sleep apnea and severe night time hypoxia. Am J Respir
Crit Care Med. 2002; 165: 67- 70.
50
60. Lavie L, Kraczi H, Hefetz A. Plasma vascular endothelial growth factor in sleep apnea
syndrome. Am J Respir Crit Care Med. 2002; 165: 1624- 1628.
61. Wormald PJ, Prescott CA. Adenoids: Comparision of radiological assessment methods with
clinical and endoscopic findings. J Laryngol Otol. 1992; 106(4): 342- 344.
62. Kemaloghi YK, Goksu N, Inal E, Akyildiz N. Radiographic evaluation of children with
nasopharyngeal obstruction due to the adenoid. Ann Otol Rhinol Laryngol. 1999; 108(1): 7-
72.$
63. Orji FT, Ezeanolue BC. Evaluation of adenoidal obstruction in children: Clinical symptoms
compared with roentgenographic assessment. The J Laryngol Otol 2008; 122: 1201 - 1205
64. Tezer MS, Karanfil A, Aktas D. Association between adenoidal- nasopharyngeal ratio and
right ventricular diastolic functions in children with adenoid hypertrophy causing upper
airway obstruction. Int J Pediatr Otorhinolaryngol. 2005; 69(9): 1169- 1173.
65. Major MP, Flores- Mir C, Major PW. Assessment of lateral cephalometric diagnosis of
adenoid hypertrophy and posterior upper airway obstruction: a systematic review. Am J
Orthod Dentofacial Orthop. 2006; 130(6): 700- 708.
66. Caylakli F, Hizal E, Yilmaz I, Yilmazer C. Correlation between adenoid- nasopharynx ratio
and endoscopic examination of adenoid hypertrophy: a blind , prospective clinical study. Int
J Pediatr Otorhinolaryngol. 2009; 73(11): 1532-1535.
67. Modrzynski M, Zawisza E. The present methods of diagnosing adenoidal hypertrophy in
children. Przegl Lek. 2003; 60(5): 383-386.
68. Paradise JL, Bernard BS, Colborn DK, Janosky JE. Assessment of adenoidal obstruction in
children: Clinical signs Versus roentgenographic findings. Pediatrics. 1998; 101(6): 979-986.
51
69. Fujioka M, Young LW, Girdany BR. Radiographic Evaluation of Adenoidal Size in
Children: Adenoidal- Nasopharyngeal Ratio. A J R 1979; 133: 401- 404.
70. Elwany S. The adenoidal- nasopharyngeal ratio (AN ratio) its validity in selecting children
for adenoidectomy. J Laryngol Otol. 1987; 101: 569- 573.
71. Caulfield HM, Obstructive sleep apnoea in childhood. In Scott- Brown’s Otolaryngology,
Vol. 1: 7th edition, (Michael G, George GB, Martin JB, et al. eds), Hodder Arnold London.
2008; 1102 – 1113.
72. Couriel J. Assessment of the child with recurrent chest infections. Br Med Bull. 2002; 1: 115-
132.
73. Araoye MO. Research methodology with statistics for health and social sciences; Nathadex
Publishers, Ilorin Nigeria, 2004: 115- 129.
74. Jean WD, Fernando DCJ, Maw AR, Leighton BCA. Longitudinal study of the growth of
nasopharynx and its contents in normal children. British J Radiol. 1981; 54: 117 – 121.
75. Jacobs IN, Gray RF, Todd NW. Upper airway obstruction in children with Down syndrome.
Arch Otolaryngol Head Neck Surg. 1996; 122(9): 945 – 950.
76. Balbani AP, Weber SA, Montovani J C. Update in obstructive sleep apnea syndrome in
children. Braz J Otorhinolaryngol 2005; 71(1): 74-80.
77. Bitar MA, Rahi A, Khalifeh M, Madanat LM. A suggested clinical score to predict the
severity of adenoid obstruction in children. Eur Arch Otorhinolaryngol. 2006; 263: 924–928
78. Duman D, Naiboglu B, Esen HS. Impaired right ventricular function in adenotonsillar
hypertrophy.Int J Cardiovasc Imaging. 2008; 24:261–267
52
APPENDIX 1
RESEARCH PROTOCOL ON STUDY OF ENLARGED ADENOIDS AND
CARDIORESPIRATORY COMPLICATIONS IN CHILDREN
SECTION A: Biodata
1. Identification No: …………..
2. Age (years): ………………….
3. Sex M ( ) F ( )
SECTION B: Medical history.
4. When did you first notice the problem? a) < 1mth b) 2- 4 months c) > 3months
5. Does your child snore while asleep? a ) Yes b ) No
6. Does your child have restless sleep? a ) Yes b ) No
7. Have your child ever stopped breathing at night? a ) Yes b ) No
8. If yes to question 10 above how often per night? a) < 10 b) > 10- 20 c) >20 d) don’t know.
9. Does your child wet bed? a ) Yes b ) No
10. Does your child regularly fall asleep during the day? a) Yes b ) No
11. If yes to 14 above for how long? a) < 30mins (b) 30mins – 1 hr (c) > 1 hr
12. Does your child mouth breathe? a ) Yes b ) No
13. Does your child have noisy breathing? a ) Yes b ) No
14. Does your child has wet nose ( nasal discharge) (a) Yes (b) No
15. Is your child growing well? (a) Yes (b)No
16. Have you noticed any other abnormality with this child (a) Yes (b) No
17. If yes to 20 above mention the one noticed.
53
SECTION C (Examination Findings)
Ear…………………
Nose……………….
Throat……………..
SECTION D (Radiological reports)
(1) X- ray PNS
Adenoidal measurement …………………….
Nasopharyngeal measurement ……………….
Adenoidal – Nasopharyngeal Ratio …………..
(2) CXR finding……………………………
SECTION E
Electrocardiographic report…………………..
54
APPENDIX 2
INFORMED CONSENT DOCUMENT
The principal investigator conducting this study is Dr Taiwo Olugbemiga ADEDEJI, a Senior
Registrar at the Department of Ear, Nose and Throat, Ladoke Akintola University of Technology
Teaching Hospital, Osogbo. He is to be contacted in case there are questions concerning the exercise.
His Telephone number is 08068830318.
Study title: Enlarged Adenoids and Cardiorespiratory Complications in Children at LAUTECH
Teaching Hospital, Osogbo
Risk: The exercise is safe and does not carry any risk.
Confidentiality: The information provided will be treated with utmost confidentiality. No third party will have access to the information that will be provided.
Voluntary nature of the study: Your participation in this study is voluntary. You have the right to withdraw from participating in the exercise at any stage of the study without any penalty.
Statement of consent: I have read or listened to the above information and the contents are well understood by me. I therefore give my consent to participate in the study.
Participant’s number……………………………………………………………
Signature / Thumbprint of participant / Date………………………………….
Signature of Investigator / Date……………………………………………….
Signature / Thumbprint of witness / Date …………………………………………..
55
APPENDIX 3: MEASUREMENT OF ADENOIDAL NASOPHARYNGEAL RATIO.
X
S P
C X
S = Spheno-basiociput Synchondrosis
XX = line along the straight part of anterior margin of Basiocciput
P = posterior- superior edge of hard palate
C = Perpendicular line from XY to greatest depth of Adenoid tissue
Adenoidal nasopharyngeal ratio = Adenoidal depth / Nasopharyngeal depth (XC/XP)
56
APPEDIX 4: PATIENT WITH SIGNIFICANT OBSTRUCTION OF THE
NASOPHARYNX BY ADENOID TISSUE
57
APPENDIX 5: PATIENT WITH COMPLETE OBSTRUCTION OF THE
NASOPHARYNX BY ADENOID TISSUE
58
APPENDIX 6: FOUR POINT CLINICAL RATING OF SCALE FOR ADENOIDAL
SYMPTOMS 63
Symptom and grade Severity
Snoring
0 Absent
1 Present on a few occasions during sleep
2 Present whenever asleep
3 Always present both asleep and awake
Mouth breathing
0 Absent
1 Present on a few occasions during sleep
2 Present whenever asleep
3 Always present both asleep and awake
Obstructive breathing during sleep
0 Absent
1 Present on a few occasions
2 < 5 episodes daily
3 ≥ 5 episodes daily
The minimum possible score = 1 and the maximum possible score = 9
Grading:
1 – 3 = mild
4 – 6 = moderate
7 – 9 = severe
59
60
61
62