1
FREQUENCY AND EFFECT OF DYSPHAGIA ON 30-DAY OUTCOME IN
ACUTE STROKE PATIENTS AT THE UNIVERSITY COLLEGE
HOSPITAL, IBADAN.
A DISSERTATION SUBMITTED TO THE NATIONAL POSTGRADUATE
MEDICAL COLLEGE OF NIGERIA IN PARTIAL FULFILMENT OF THE
AWARD OF THE FELLOWSHIP OF THE COLLEGE IN INTERNAL
MEDICINE (IN THE SUBSPECIALTY OF NEUROLOGY).
OLAJIDE, OLABODE TEMITOPE.
M.B, B.S. (LAGOS) 2002.
NOVEMBER 2015
2
DECLARATION
It is hereby declared that this work is original unless otherwise acknowledged. The work has
neither been presented to any other college for an award nor has it been submitted elsewhere for
publication.
Candidate Signature: ……………………………………………..
Date: ……………………………………………
3
CERTIFICATION
The study reported in this dissertation was carried out by the candidate, Dr OLAJIDE, Olabode
Temitope, under my supervision.
I have also supervised the writing of the dissertation to my satisfaction and authorized the
submission of the work for the Fellowship Examination in the Faculty of Internal Medicine.
Principal Supervisor
Signature ……………………………………………………………………..
Name of Supervisor ………………………………………………………………….
Status of Supervisor ……………………………………………………………………
Year of Fellowship in the Faculty ………………………………………………………
Date ………………………………………………………………………………
4
ATTESTATION
I certify that the work reported in this dissertation was carried out by
………………………………………………………………………………. In the Department
of Medicine and under the supervision of
………………………………………………………………………………
Address ………………………………………………………………………………
Name …………………………………………………………………………………..
Signature …………………………………………………………………………………
Designation …………………………………………………………………………….
Date ………………………………………………………………………………………….
5
DEDICATION
This work is dedicated unto the King eternal, immortal, invisible, the only wise GOD.
6
ACKNOWLEDGEMENT
My deep appreciation goes to my teacher and supervisor, Prof. A. Ogunniyi, for his astute
attention to detail in the conduct and write up of this project as well as his rare display of
commitment to this work, his fatherly tutelage and immense assistance at every point of writing.
My immense appreciation also goes to Dr M.O. Owolabi, Dr Ipadeola and Dr A. Ayodele for
reading through this work constructively and promptly.
I am grateful to my numerous patients who willingly allowed me to examine them and use some
of their investigation results.
My appreciation also goes to all my teachers and trainers in the residency programme who taught
me what I needed to know. And to my fellow residents in the department of medicine who
always informed me of new stroke patients in the hospital, I say thank you.
I am eternally grateful to my wife, Foluso, who encouraged, supported and showed great
understanding during this project. And to our children who allowed me to concentrate on the
work, I say thank you.
To the Almighty God, my hope and my strength, without you this work would have been totally
impossible. Thank you, LORD.
7
TABLES OF CONTENT
Declaration……………………………………………………..............ii
Certification……………………………………………………………iii
Attestation by Head of Department……………………………………iv
Dedication……………………………………………………………...v
Acknowledgements…………………………………………………….vi
List of Tables…………………………………………………………...viii
List of figures…………..……………………………………………….ix
Abbreviation…………………………………………………………….x
Abstract…………………………………………………………………xi
Chapter 1: Introduction…………………………………………………1
Chapter 2: Literature Review……………………………………………7
Chapter 3: Materials and Method……………………………………….25
Chapter 4: Results……………………………………………………….35
Chapter 5: Discussion……………………………………………………53
Chapter 6: Conclusion……………………………………………………63
Recommendation………………………………………………………...65
Limitations……………………………………………………………… 66
References……………………………………………………………….67
Appendix 1-4…………………………………………………………… 85-95
Informed consent………………………………………………………….96
8
LIST OF TABLES
Table 1: GCS and NIHSS of study participants
Table 2: Clinical Characteristics of the Study Population
Table 3:Comparison of laboratory parameters between Cases and Controls
Table 4: Frequency of dysphagia among stroke admissions during study period.
Table 5: Distribution of stroke types in dysphagic and non-dysphagic stroke patients.
Table 6: Distribution of vascular territories involved in dysphagic and non-dysphagic stroke
Table 7: Stroke lesion sites in study participants.
Table 8: Frequency of complications observed in study participants.
Table 9: Outcome of dysphagic and non-dysphagic stroke patients.
Table 10:Outcome of patients with dysphagia alone and patients with dysphagia and aspiration
pneumonia.
Table 11: Outcome of dysphagic and non-dysphagic stroke patients using Modified Rankin
Scale (MRS) and Barthel Index (BI)
Table 12: comparison of outcome of stroke patients with dysphagia alone and outcome of stroke
patients with dysphagia complicated by aspiration pneumonia using Modified Rankin Scale
(MRS) and Barthel Index (BI)
Table 13: Univariate and Multivariate Binary logistic regression analysis to assess the
determinants of 30- day case fatality.
Table 14:COX Proportional Hazard Model for Patients with Dysphagia controlling for the
effect of sepsis
9
LIST OF FIGURES
Figure 1: Comparison of gender distribution in dysphagic and non-dysphagic stroke
patients
Figure 2:Kaplan-Meier survival curve for cases and control.
Figure 3: Kaplan-Meier survival curve for patient with dysphagia without aspiration and those
with aspiration
10
LIST OF ABBREVIATIONS
GCS: Glasgow Coma Scale
NIHSS: National Institute of Health Stroke Scale
TACS: Total Anterior Circulation Syndrome
PACS: Partial Anterior Circulation Syndrome
POCS: Posterior Circulation Syndrome
BI: Barthel index
MRS: Modified Rankin scale
ECG: Electrocardiography
CN: Cranial Nerves
SD: Standard Deviation
HDL: High density lipoprotein
LDL: Low density lipoprotein
WST: Water swallowing test
RBS: Random blood sugar
CXR: Chest X-ray
11
ABSTRACT
Background: Dysphagia is common after acute stroke and can directly affect patient’s prognosis
and recovery through development of chest infection. This study intended to highlight how
common are dysphagia and aspiration pneumonia in acute stroke patients, and their impact on
the outcome of acute stroke patients in our environment. Few studies have been done in our
environment to look at the frequency of dysphagia and its impact on outcome in acute stroke
patients.
Objective: To determine the frequency of dysphagia and its effect on 30-day outcome in acute
stroke patients. Also to determine the association, if any, between dysphagia and stroke type,
stroke severity, lesion site, and/ or lesion size and to determine the frequency of aspiration
pneumonia in acute stroke with and without dysphagia, and itseffect on 30 day outcome in acute
stroke patients.
Materials and Methods: A total of 200 stroke patients were recruited. Assessment of dysphagia
using Bedside Swallowing Test was done for all the patients. There were ninety nine (99)
dysphagic stroke patients and one hundred and one (101) non-dysphagic stroke patients. NIHSS
and GCS were determined on admission.Using a questionnaire, socio-demographic characteristic
and detail of past medical history were obtained. Patients’ functional outcomes were assessed
using Modified Ranking scale and Barthel index at one week, two weeks and one month after
stroke. Aspiration pneumonia was diagnosed based on the established criteria. Strokes were
classified according to brain CT scan result.All data was analyzed using Statistical Package for
Social Sciences (SPSS) version 16
12
Results: The mean age of study participants was 60.8± 11.8 years. Male to female (M: F) ratio
was 1.08: 1.0.Out of 200 patients that were recruited for this study, 100 had ischaemic stroke
subtype and 100 had haemorrhagic stroke. The frequency of dysphagia in this study was 46.47%
when assessed by measuring peripheral oxygen desaturation and 48.50% when assessed with
10mls water swallowing test. Haemorrhagic stroke type was associated with dysphagia in acute
stroke patients in this study. . Stroke lesions in the subcortical regions were more associated
with dysphagia than cortical lesions. Baseline severe NIHSS was associated with dysphagia. The
size of stroke lesion was also associated with dysphagia. Stroke patients with large lesion sizes
had increased propensity to develop dysphagia. 78.9% of stroke patients with dysphagia died on
admission with their average survival days shorter than those without swallowing difficulty.
Dysphagic stroke patients had worse functional outcome at the end of 4th week based on the
MRS and BI values. 30-day case fatality rate for patients with dysphagia alone was 24. 2%. The
frequency of aspiration pneumonia in stroke patients with dysphagia in this study was 62.6%.
69.4% of patients with aspiration pneumonia died on admission with the average survival days
much shorter than those without aspiration pneumonia. Functional outcome based on MRS and
BI values at 4th week was worse in patients with aspiration pneumonia. 30-day case fatality rate
for dysphagic stroke patients complicated by aspiration pneumonia was 55.6%. In the
multivariate regression analysis, dysphagia (P= 0.005), aspiration pneumonia (p= 0.024), severe
baseline NIHSS (p= 0.049), and haemorrhagic stroke subtype (p= 0.043) were important
determinants of 30-day case fatality in this study.
Conclusion: Swallowing function should be assessed in all acute stroke patients because
swallowing dysfunction is common and complications frequently arise. Pneumonia risk is
greatest in patients with dysphagia and has negative impact on the outcome of acute stroke
13
patients. Predictors for dysphagia were lesion size, haemorrhagic stroke, initial severe NIHSS
score, and subcortical lesions. Dysphagia and aspiration pneumonia were significant
determinants of 30-day case fatality.
14
CHAPTER 1
INTRODUCTION
Ischemic stroke is defined as an episode of neurological dysfunction caused by focal cerebral,
spinal, or retinal infarction lasting more than 24hrs or death, and other etiologies excluded.1
Stroke caused by intracerebral cerebral hemorrhage is defined as a rapidly developing clinical
signs of neurological dysfunction attributable to a focal collection of blood within the brain
parenchyma or ventricular system that is not caused by trauma.1
It has significant economic, social and medical complications worldwide.2 Stroke is a leading
cause of death, disability, dementia and depression.3 Sub-Saharan Africa is undergoing
epidemiological transition with stroke and other cardiovascular diseases increasingly
contributing to the burden of disease.4 Stroke is increasingly becoming a major cause of death
and morbidity in African population5. It has an annual incidence rate of up to 316 per 100 000, a
prevalence rate of up to 315 per 100,000, and a 3- year fatality of up to 84% in Africa.6 It is a
leading cause of neurological admission in some tertiary hospitals in Nigeria, responsible for
0.92% - 4% of hospital admission.7 A study done at the University of Nigeria Teaching Hospital,
Enugu showed that neurological admission was responsible for 14.8% of medical admission and
stroke responsible for 64.9% of the neurological admissions.8 Another study in Ibadan showed
that stroke was responsible for 50.4% of neurological admissions at the University college
Hospital, Ibadan.9 A report by Danesi, et al in 2007 showed that the prevalence rate of stroke in
urban Nigeria was 1.14/1,000.10 The study concluded that the prevalence rate was lower than
those in most developed countries and this may be related to lower incidence and higher stroke
15
mortality in developing countries.10 The incidence of stroke in Nigeria is likely to be rising and
the mortality increasing.
Patients who have had an acute stroke are at risk of developing a wide range of complications.
These are important because they may cause death or delay successful rehabilitation. Studies
have shown that death within a few days of stroke is a direct consequence of brain damage.
However, those occurring over the following weeks are usually due to potentially preventable
problems such as infection, venous thromboembolism, cardiac diseases, aspiration, pressure
sores, depression, etc.11-15 Presence of complications has been associated with poor stroke
outcome in Nigeria.16, 17
Dysphagia after stroke is common and its detection is an important part of acute stroke
management. Literature suggests that dysphagia can affect 19-81% of stroke patients.18-21
Dysphagia was considered a significant gastrointestinal complication in stroke survivors.22 A
study done in South Africa showed a prevalence of 56%.23
Dysphagia is considered to be present when there is difficulty in swallowing, food is stuck in the
mouth and throat, or presence of cough after swallowing. Other features include impaired voice
or abnormal pulse oximetry during water swallowing test.24 Swallowing disorder can be divided
into oropharyngeal dysphagia and eosophageal dysphagia. The most common cause of
oropharyngeal dysphagia is cerebrovascular accident. Other causes of dysphagia are brain
tumour, brain injury, bulbar and pseudobulbar palsy, neurodegenerative diseases such as
amyotrophic lateral sclerosis, multiple sclerosis, multiple system degenerations, Parkinson’s
16
disease, Huntington’s disease, myasthenia and myasthenic syndromes, and peripheral
neuropathies.25, 26 Dysphagia after stroke is associated with respiratory complications, increased
risk of pneumonia, nutritional compromise, and dehydration. It also reduces quality of life.27
Length of hospitalization is increased in stroke patients with dysphagia, and these individuals are
more likely to be discharged to nursing homes compared with stroke patients without
dysphagia.28 Fortunately, there is emerging evidence that early detection of dysphagia reduces
not only pulmonary complication, but also length of hospital stay and overall healthcare cost for
acute stroke patients.29, 30
Patients’ awareness of their disabilities, including dysphagia after stroke, represents an
important aspect of functional recovery. Patients’ with poor awareness experienced more
complications of dysphagia.31, 32
Africa bears a heavy burden of stroke and there is severe scarcity of facilities and human
resources for prevention, investigations, acute care and rehabilitation. Identifying and treating
stroke patients at risk for dysphagia are extremely important and this could be effective in
reducing morbidity and mortality in our environment.
17
1.1 JUSTIFICATION FOR THE STUDY
Stroke is increasingly contributing to the burden of disease worldwide and becoming a major
cause of death and morbidity in African population.4, 5 Globally, it is the second leading cause of
death and 87% of deaths are recorded in developing countries.6, 33 Occurrence of dysphagia after
stroke is common and aspiration pneumonia resulting from dysphagia has been identified as one
of the most important complications contributing to morbidity and mortality in acute stroke
patients. With insufficient and limited resources available, complicated by the poor
infrastructural back-up in most hospitals in sub-Saharan Africa, prevention, early detection, and
aggressive intervention to treat aspiration pneumonia may reduce the unacceptably high
mortality rate of stroke in our environment. Furthermore, early detection of dysphagia reduces
not only pulmonary complication, but also length of hospital stay and overall healthcare cost for
acute stroke patients.
Bedside clinical swallowing tests are frequently used to detect swallowing difficulty in acute
stroke patients. These assessments are perceived as simple, quick to perform and can be repeated
frequently. Availability of Videofluoroscopy (VF) and Fiberoptic Endoscopy Evaluation of
Swallowing (FEES), considered as gold standards, are limited universally in many clinical
settings, especially in Sub-Saharan Africa, where stroke patients are managed.
This study will further highlight the importance of screening for dysphagia in acute stroke
patients using bedside swallowing assessments, thereby curtailing the attending complication.
Moreover, there is a paucity of published data on incidence and impact of dysphagia in acute
stroke patients in our environment. This study will contribute to the existing literature and reduce
our dependence on foreign data for our medical practice in this regard.
18
1.2 AIMS AND OBJECTIVES
19
General
To determine the frequency of dysphagia and its effect on 30-day outcome in acute stroke
patients.
Specific
1. To determine the frequency of dysphagia in acute stroke patients.
2. To determine the association, if any, between dysphagia and stroke subtype
(haemorrhagic/Ischaemic), stroke severity, and lesion site (cortical, subcortical, brainstem
/ cerebellum)
3. To determine the relationship of dysphagia in acute stroke to short term outcome (30 days
post stroke) i.e. case fatality rate and functional outcome in survivors
4. To determine the frequency of aspiration pneumonia in acute stroke with and without
dysphagia.
5. The relationship of aspiration pneumonia to 30 day outcome (case fatality rate and
functional outcome in survivors).
CHAPTER 2
20
LITERATURE REVIEW
2.0 Definition of stroke
Stroke is classically characterized as a neurological deficit attributed to an acute focal injury of
the central nervous system by a vascular cause.1 Modern definitions of stroke, which was
published in 2013, were formalized based on advances in basic science, neuropathology and
neuroimaging.1
Ischaemic stroke is defined as an episode of neurological dysfunction caused by focal cerebral,
spinal, or retinal infarction.1
Stroke caused by intracerebral hemorrhage is defined as rapidly developing clinical signs of
neurological dysfunction attributable to a focal collection of blood within the brain parenchyma
or ventricular system that is not caused by trauma.1
Stroke caused by subarachnoid hemorrhage is defined as rapidly developing signs of
neurological dysfunction and/or headache because of bleeding into the subarachnoid space,
which is not caused by trauma.1
Stroke caused by cerebral venous thrombosis is defined as infarction or hemorrhage in the brain,
spinal cord, or retina because of thrombosis of a cerebral venous structure.1
2.1 Epidemiology of stroke in Nigeria
21
The looming epidemic of stroke and other chronic non-communicable diseases associated with
lifestyle and demographic transitions occurring all over the world is increasingly being
acknowledged, especially in Sub-Saharan Africa.34
Stroke is a major leading cause of death and a major cause of morbidity and mortality
worldwide.35 Globally, it is the second leading cause of death and 87% of deaths are recorded in
developing countries.6, 33 In the USA, stroke has moved from the second to the third leading
organ- and disease-specific cause of death.36 This is due to improved vascular risk reduction
therapies and acute stroke management approaches. However, stroke still remains the second
leading cause of cardiovascular deaths worldwide after Ischaemic heart disease.36 According to
the data from global burden of disease in 2010, stroke was the third leading cause of disability-
adjusted life years (DALY) worldwide as compared to its fifth position in 1990.37
Sub-Saharan Africa is undergoing epidemiological transition with stroke and other vascular
diseases increasingly contribute to the burden of disease.4 Stroke has a significant economic,
social and medical burden on low resource countries including Nigeria.2, 38, 39 In Nigeria, the
case fatality rates in a study by Ogun et al were: 9% at 24 hours; 28% at 7 days; 40% at 30 days;
and 46% at 6 months.2 Another study documented 23.8% as 30-day case fatality.40 The
prevalence of stroke in urban Nigeria is 1.14/1000.10. A crude incidence rate in urban Nigeria
was 25.2 per 100,000 per year (21.6- 28.8/100,000).41 A study done at the University of Nigeria
Teaching Hospital, Enugu showed that neurological admission was responsible for 14.8% of
medical admission and stroke responsible for 64.9% of the neurological admissions.8 A study
22
showed that stroke was responsible for 50.4% of neurological admissions at the University
college Hospital.9 A study by Komolafe et al showed that stroke was responsible for 3.6% of all
medical admissions with a case fatality rate of 45% and the majority of death occurring in the
first week.42
2.2 Classification of stroke
Stroke can be classified as ischemic or hemorrhagic. Hemorrhagic strokes may involve the brain
parenchyma (intracerebral hemorrhage [ICH]), the subarachnoid space or the ventricular
system.43 TOAST (Trial of Org 10172 in Acute Stroke Treatment) Classification of ischemic
stroke grouped ischemic stroke into five subtypes: large artery atherosclerosis, cardio–aortic
embolism, small artery occlusion (lacunae), stroke of other determined etiology, and stroke of
undetermined etiology.44 The Oxford Community Stroke Project (OCSP) classification (usually
abbreviated as the Oxford classification) defines four subcategories of cerebral infarction on the
basis of likely clinical localization of the infarct topography based on the clinical assessment of
the presenting signs and symptoms. These are total anterior circulation stroke (TAC), partial
anterior circulation stroke (PAC), lacunar stroke (LAC), and posterior circulation stroke (POC).45
2.3 Risk factors for stroke
The identification and recognition of risk factors for stroke is important for the primary
prevention of stroke. Risk factors are generally divided into two categories: modifiable and non-
modifiable risk factors. Age, gender and ethnicity are non-modifiable risk factors for stroke.
23
Modifiable or potentially modifiable risk factors include a number of physiological and
environmental factors. These include hypertension, smoking, diabetes, heart disease, poor
nutrition, physical inactivity and obesity.46, 47
2.4 Evaluation of acute stroke
Early investigations in acute stroke patients include non-contrast brain CT or brain MRI, blood
glucose, serum electrolytes/ renal function tests, electrocardiogram (ECG), markers of cardiac
ischaemia, complete blood count, including absolute platelet count, prothrombin time/
international normalized ratio (INR), activated partial thromboplastin time, Oxygen saturation
and chest radiography.48, 49
2.5 Goals of management of acute stroke
Acute ischemic stroke management guidelines include cardiorespiratory resuscitation, urgent
accurate diagnosis and classification, emergency recanalization, optimisation of cerebral
perfusion, cardiovascular risk profiling and control of vascular risk factors (secondary
prevention), prevention, early detection and management of complications, and early
rehabilitation.49
Spontaneous intracerebral hemorrhage management guidelines include cardiorespiratory
resuscitation, urgent accurate diagnosis and classification, prevention of hematoma expansion/
aspiration of clot optimisation of cerebral perfusion, cardiovascular risk profiling and control of
24
vascular risk factors (secondary prevention), prevention, early detection and management of
complications, and early rehabilitation.48
2.6 Complications of Stroke
Acute stroke patients are at risk of developing a wide range of complications. Complications that
occur within the first week of stroke are cerebral oedema, increased intracranial pressure,
transtentorial herniation, seizures, aspiration pneumonia, hyperglycaemia, cardiac arrhythmia,
and inappropriate antidiuretic hormone secretion. However, those occurring over the following
weeks are usually due to potentially preventable problems such as infection, venous
thromboembolism, cardiac diseases, aspiration, pressure sores, depression, etc.11-15 Medical
complication may directly or indirectly affect clinical outcome, including length of hospital
stay50, 51 and increased mortality.52-54 Medical and neurological complications have in previous
studies been linked with at least 50% of deaths in the early phase following stroke. 53 55 56 57
Presence of complications has been associated with poor stroke outcome in Nigeria.16, 17
2.7 Dysphagia after stroke
Dysphagia after stroke is common, and its detection is an important part of acute stroke
management.20 The most frequent complications of dysphagia are increased mortality,
pulmonary risk such as aspiration pneumonia, dehydration, malnutrition, and prolonged
hospitalization.19, 20 Surveys have shown that the predictors of dysphagia in clinical assessments
include older age, greater severity of stroke, wet vocal quality, abnormal palatal reflex, weak or
25
absent cough, abnormal voluntary cough, coughing with swallowing and injury sustained in
controlling secretions.20, 58 Because of the bilateral upper motor neuron innervation of most of
the lower cranial nerves involved in swallowing, many published studies state that the
mechanism of deglutition is not significantly affected by damage to a single cerebral hemisphere.
Recently, however, it has been pointed out that unilateral hemispheric strokes do affect lower
cranial nerve function in general and swallowing in particular.59-61
The intricate mechanism of swallowing can be divided into three phases: oral, pharyngeal, and
eosophageal. Dysphagia is a disruption in the swallowing process, which include difficulty in
transporting (or a lack of transporting) a food or liquid bolus from the mouth through the
pharynx and esophagus into the stomach.26 Since the main function of swallowing is the safe
delivery of a food bolus into the stomach, then the immediate complication of dysphagia is food
entering the airway.62
Causes of disruptions in the swallowing process can be divided into superior (oropharyngeal)
and inferior (eosophageal). Oral factors that contribute to dysphagia include inability to hold
food in the mouth due to reduced lip closure, inability to hold a bolus due to reduced tongue
shaping and coordination, inability to align teeth due to reduced mandibular movement, delayed
oral onset of swallow due to apraxia of swallow or reduced oral sensation, presence of food
residue on the tongue due to reduced tongue range of movement or strength, reduced tongue
elevation, oral infection and trauma during resuscitation. Pharyngeal factors that contribute to
dysphagia include delayed pharyngeal swallow, nasal penetration during swallow due to reduced
velopharyngeal closure, coating of pharyngeal walls after the swallow due to bilateral reduction
of pharyngeal contraction, and delayed pharyngeal transit time.63
26
Neurologic dysphagia may be caused by a disruption in different parts of the central nervous
system (supranuclear level, level of motor and sensory nuclei taking part in swallowing process,
peripheral nerves level and a pathology of muscle cells and spindles) or neuromuscular and
muscular disorders.
Neurologic disorders causing dysphagia include stroke, brain tumors, brain injury, bulbar and
pseudobulbar paralysis, neurodegenerative diseases (amyotrophic lateral sclerosis, multiple
sclerosis), tabes dorsalis, multisystem degenerations, Parkinson's disease, delayed dyskinesia,
Huntington's disease, myasthenia and myasthenic syndromes, myopathies and peripheral
neuropathies.26 Aspiration, which is the incursion of food material into the airway and below the
true vocal cords, is one of the most important consequences of dysphagia along with
malnutrition.62
2.8 Incidence and Prevalence of dysphagia after stroke.
Swallowing disorders after a stroke are common. The incidence ranges from 18% to 81% in the
acute phase and with prevalence of 12% among such patients.19, 20, 59, 62, 64 A study done in South
Africa showed a prevalence of 56%. 23
27
2.9 Normal control of swallowing
Swallowing is a complex neuromuscular activity consisting essentially of three phases: oral,
pharyngeal and esophageal phase. Each phase is controlled by a different neurological
mechanism. The oral phase, which is entirely voluntary, is mainly controlled by the medial
temporal lobes and limbic system of the cerebral cortex with contributions from the motor cortex
and other cortical areas. The pharyngeal swallow is started by the oral phase and subsequently is
coordinated by the swallowing center on the medulla oblongata and pons. The reflex is initiated
by touch receptors in the pharynx as a bolus of food is pushed to the back of the mouth by the
tongue, or by stimulation of the palate (palatal reflex). The autonomic nervous system
coordinates the pharyngeal and esophageal phases. The neural control of swallowing is
commonly divided into three elements— an afferent system, consisting of cranial nerve fibres V,
V11, IX, and X, providing swallow sensory feedback; the brainstem swallowing centre or central
pattern generator, reflexly coordinating swallowing via the V, V11, IX, X, XII motor nuclei; and
higher centres, including the frontal cortex, which initiate and modulate volitional swallowing.
During oral phase, food is moistened by saliva followed by process of mastication. The bolus is
ready for swallowing when it is held together by saliva, sensed by the lingual nerve of the tongue
(V3). In order for anterior to posterior transit of the bolus to occur, orbicularis oris contracts and
adducts the lips to form a tight seal of the oral cavity. The intrinsic muscles of the tongue,
controlled by cranial nerve XII, contract to make a trough (a longitudinal concave fold) at the
back of the tongue. The tongue is then elevated to the roof of the mouth by the mylohyoids,
genioglossus, styloglossus and hyoglossus such that the tongue slopes downwards posteriorly.
Next, the superior longitudinal muscle elevates the apex of the tongue to make contact with the
28
hard palate and the bolus is propelled to the posterior portion of the oral cavity. Once the bolus
reaches the palatoglossal arch of the oropharynx, the pharyngeal phase, which is reflex and
involuntary, then begins. Receptors initiating this reflex are proprioceptive (afferent limb of
reflex is IX and efferent limb is the pharyngeal plexus- IX and X).
For the pharyngeal phase to work properly all other outlets from the pharynx must be occluded—
this includes the nasopharynx and the larynx. When the pharyngeal phase begins, other activities
such as chewing, breathing, coughing and vomiting are concomitantly inhibited.65
Like the pharyngeal phase of swallowing, the esophageal phase of swallowing is under
involuntary neuromuscular control. However, propagation of the food bolus is significantly
slower than in the pharynx. The bolus enters the esophagus and is propelled downwards first by
striated muscle, controlled by recurrent laryngeal and cranial nerve X, then by the smooth muscle
(X) at a rate of 3–5 cm/s. The upper esophageal sphincter relaxes to let food pass, after which
various striated constrictor muscles of the pharynx as well as peristalsis and relaxation of the
lower esophageal sphincter sequentially push the bolus of food through the esophagus into the
stomach. Finally, the larynx and pharynx move down from the hyoid to their relaxed positions by
elastic recoil.
Swallowing therefore depends on coordinated interplay between many various muscles, and
although the initial part of swallowing is under voluntary control, once the deglutition process is
started, it is quite hard to stop it.65-68
29
2.10 Pathophysiology of dysphagia after stroke.
Swallowing is usually thought to be the result of local peristaltic mechanisms in the esophagus,
combined with reflex involvement of swallowing centers in the brainstem. However, the cerebral
cortex appears to play a critical role in the initiation of voluntary swallowing.69 Dysphagia in
stroke is usually considered to indicate a brain stem lesion caused by vertebrobasilar disease or
bilateral corticobulbar fibre damage.59 However, it has also been reported in unilateral
hemispheric stroke.70, 71 Neuropathological examination of dysphagic stroke patients either at
necropsy or with magnetic resonance imaging has shown that, in many cases, the lesion is
discrete and unilateral.72 A study showed that stroke in only one hemisphere is a more common
cause of dysphagia than is generally believed.59 Injury to swallowing motor areas and/or their
connection to the brainstem will usually result in dysphagia. The most common cause of this is
stroke. Swallowing disorders are frequently associated with life - threatening complications of
pulmonary aspiration and malnutrition.59
Voluntary control of mastication and bolus transport during the oral phase can be interrupted by
cerebral lesions.73, 74 Cortical lesions involving the precentral gyrus may produce contralateral
impairment in facial, lip, and tongue motor control, and contralateral compromise in pharyngeal
peristalsis.60 Cerebral lesions causing impairment in cognitive function such as concentration or
selective attention may also impair control of swallowing.75 Brain stem strokes are less common
than cortical lesions but result in the largest swallowing compromise.19, 76 Brain stem lesions can
affect sensation of the mouth, tongue, and cheek, timing in the trigger of the pharyngeal swallow,
laryngeal elevation, glottic closure, and cricopharyngeal relaxation.60, 77 Regardless of lesion
location, because stroke is more common in the elderly,78 normal age-related swallowing
disorder could further compound stroke-related dysphagia. The elderly post stroke patient might
30
no longer be able to compensate for normal changes in skeletal muscle strength that reduce
mastication65 or diminish lingual pressure.79 Therefore, single or multiple aspects of the swallow
may be impaired depending on stroke type and patient age.19 Using Transcranial Magneto-
electric Stimulation (TCMS), a safe, non-invasive, method for studying the physiology of the
human central nervous system, the corticofugal projections to the muscles active in swallowing
have been identified 80, 81_ENREF_58 and shown that oral muscles, such as the mylohyoids are
represented
symmetrically between the two hemispheres, whereas muscles of the pharynx and oesophagus
are represented very asymmetrically, with most individuals having a dominant swallowing
hemisphere, independent of handedness.72 The process of swallowing involves a complex
sequence of neuromuscular events that transport food from mouth to stomach whilst ensuring
protection of the airway. Its neural control is commonly divided into three elements— an
afferent system, consisting of cranial nerve fibres V,V11, IX, and X, providing swallow sensory
feedback; the brainstem swallowing centre or central pattern generator, reflexly coordinating
swallowing via the V, V11, IX, X, XII motor nuclei; and higher centres, including the frontal
cortex, which initiate and modulate volitional swallowing.82, 83 The importance of the cortex in
the control of swallowing is well recognized.68 A study showed that patients dysphagic after
unilateral hemisphere stroke have smaller pharyngeal responses from the unaffected hemisphere
than do non- dysphagic patients, irrespective of the side and level (cortical or subcortical) of the
lesion.69, 72 One possible explanation for this difference is that the smaller responses are a
reflection of the asymmetrical motor representation81, 84 of pharyngeal function on the cerebral
cortex. In other words, with damage to the hemisphere containing the predominant pharyngeal
centre, swallowing cannot be maintained by the smaller pharyngeal center in the unaffected
31
hemisphere. That same study showed that the pharyngeal phase of swallowing is the most
important clinical determinant of aspiration in stroke populations85, 86
2.11 Brain lesion location in stroke and occurrence of dysphagia
Unilateral cortical lesions are associated with dysphagia in ischemic stroke.18 Functional and
anatomic imaging studies have identified several sites important to swallowing, including the
primary sensorimotor cortices, insula, anterior cingulate, internal capsule, basal ganglia,
thalamus, and cerebellum.74, 87-91 The internal capsule serves to functionally connect cortical and
brain stem nuclei via the cortical bulbar tracts. Vascular injury to these white matter tracts has
been associated with oropharyngeal deficits in swallowing. 92 The insular cortex is thought to
serve a variety of functions, including sensory and motor integration between primary cortex and
other subcortical (thalamic) nuclei or limbic areas. Other functions include a role in gustatory
sensation, visceral motor activity, and motor association. Activation of the insular cortex during
swallowing tasks may be linked to its visceral motor and integrative functions.93 The functional
roles of nuclei of the thalamus are heterogeneous, with some nuclei serving as relays for cortical
areas and others generally serving as association areas.94, 95 The globus pallidus projects to the
ventral anterior group of the thalamus, which then projects to the primary motor and
supplementary motor cortices. The ventral posterior group is primarily involved with
somatosensory integration, receiving input from the spinothalamic and trigeminal tracts and
projecting to the primary somatosensory cortex. The pulvinar, as an association nucleus,
maintains reciprocal connections to the temporal, parietal, and occipital lobes for integration of
sensory information and cognitive and visual association functions. Activation of thalamic nuclei
32
during swallowing tasks indicates the necessary role of sensory and motor input processing via
thalamocortical or thalamostriatal pathways in swallowing.89
The supplementary motor area, represented in the superior and middle frontal gyri, is believed to
be associated with motor planning and, in particular, with planning of sequential movements, as
occurs with swallowing.96 Disruption of cortical-cortical and cortical-subcortical white matter
connections, specifically periventricular white matter (PVWM) lesions, seems to increase the
risk of dysphagia and aspiration by lowering the threshold of input to the medullary swallowing
center.87 A study shows that swallowing disorders were more common with left hemispheric
stroke with left hemispheric periventricular white matter (PVWM) identified as a major site of
acute brain injury associated with dysphagia.18 The PVWM, which is the white matter adjacent
to the body of the lateral ventricles, is important in the neural control of swallowing. Ascending
somatosensory and descending motor fibers as well as intrahemispheric corticocortical pathways
are segregated within the PVWM.97 Descending corticospinal fibers from the mouth/face
representation within the ventrolateral precentral gyrus (motor cortex) are located anterolaterally
in the PVWM. Ascending sensory and descending motor pathways cross these levels and
interconnect with specific cortical, subcortical, and brain stem regions involved in swallowing.18
Ideally, Neuroimaging obtained to ascertain stroke should function as a tool to risk-stratify
patients as to the possibility of dysphagia and dysphagia complications. With the availability of
current MRI techniques, including diffusion (DWI) and perfusion weighting (PWI), areas of
infarction and dysfunctional areas as a result of hypoperfusion in the brain tissues surrounding
the infarctive areas can be easily delineated.98
33
2.12 Assessment of dysphagia in acute stroke patients
Early detection of dysphagia after stroke is an important part of acute stroke management.
Diagnosis of dysphagia begins with suspecting its presence. When dysphagia is suspected,
patients with high risk should be screened by means of simplified bedside swallowing tests.
Videofluoroscopy (VF) and fiberoptic endoscopic evaluation of swallowing (FEES) are well-
validated investigations of swallowing and they are considered as gold standards for assessment
of swallowing.20, 99 However, the most frequently used swallow test is the bedside clinical
swallowing assessments. Availability of VF and FEES is limited universally in many clinical
settings in which stroke patients are managed. Therefore the bedside clinical swallowing
assessments (BSA) have become widely used initial tests to screen for dysphagia.
The assessments are perceived as simple, quick to perform and can be repeated frequently.20
The bedside swallowing tests are gag reflex, water swallowing test and pulse oximetry.19, 100
2.12.1 Fiberoptic endoscopic evaluation of swallowing (FEES) is safe and effective for
assisting in swallowing evaluation. The patient is seated comfortably. A flexible fiberoptic
endoscope is introduced transnasally to the patient's hypopharynx where the clinician can clearly
view laryngeal and pharyngeal structures. The patient is then led through various tasks to
evaluate the sensory and motor status of the pharyngeal and laryngeal mechanism. Food and
liquid boluses are given to the patient so that the integrity of the pharyngeal swallow can be
determined. Information obtained from this examination includes ability to protect the airway,
the ability to sustain airway protection for a period of several seconds, the ability to initiate a
prompt swallow without spillage of material into the hypopharynx, timing and direction of
34
movement of the bolus through the hypopharynx, ability to clear the bolus during the swallow,
presence of pooling and residue of material in the hypopharynx, timing of bolus flow and airway
protection, sensitivity of the pharyngeal/laryngeal structures and the effect of anatomy on the
swallow.101-103
2.12.2 Videofluoroscopy (VF) is an X-ray that looks at the way swallowing works. The studies
are captured using fluoroscopy in video or digitized format that allows detailed analysis of the
oropharyngeal swallowing process. The patient is seated in front of an X-ray machine. Earrings,
necklaces and zipped tops are removed from the patient before the test as they can interfere with
the X-ray image. Food and drinks, mixed with contrast (Barium), of different consistencies are
given to the patient to swallow. The x-ray machine is only turned on during swallowing so that
the patient does not get too much radiation. All studies are started with the patient in the lateral
view where aspiration is most efficiently detected, and then finished with an anterior-posterior
view to assess swallow symmetry and vocal cord function. A video recording is also made
during the test. The procedure takes about 30 minutes.104
2.12.3 The pharyngeal reflex or gag reflex is a reflex contraction of the back of the throat
evoked by touching the soft palate or sometimes the back of the tongue. The afferent limb of the
reflex is supplied by the glossopharyngeal nerve (cranial nerve IX), which inputs to the nucleus
solitarius and the spinal trigeminal nucleus, and the efferent limb is supplied by the vagus nerve
(cranial nerve X) from the nucleus ambiguus.105 Studies have suggested that an absent gag reflex
is predictive of aspiration106-108 but refuted by others.109, 110
35
2.12.4 Pulse oximetry is a noninvasive method of bedside swallow testing.20, 111 Desaturation
during swallowing may help to identify aspiration in stroke patients. It has been suggested that
aspiration causes reflex bronchoconstriction and therefore ventilation-perfusion imbalance,
leading to hypoxia and desaturation.112 Others have suggested that abnormal swallowing leads to
poor breathing and ventilation-perfusion mismatching because of reduced inspiratory volumes.113
Using pulse oximetry for the assessment of dysphagic patients is based on the principle that
reduced and oxygenated hemoglobin exhibit different absorption characteristics to red and
infrared light emitted from a finger (or earlobe) probe.111 Oxygen desaturation ≥2% was
considered to be clinically significant.111, 114-116
2.12.5 Difficulty in drinking small volumes of water has been used to screen for dysphagia
in stroke patient.59, 106, 110, 116-118 Presence of involuntary cough, choking, change in voice
quality, drooling, respiratory difficulty and delayed swallowing are considered to be abnormal
and indicative of swallowing difficulty.20, 72, 100, 119, 120 Studies showed that sensitivity of water
swallowing test in detecting swallowing difficulty ranged from 20.8% - 85.5% and specificity
ranged from 50% -98.75%.114-116, 121, 122 A study showed that sensitivity and specificity of
cough/ voice change in detecting dysphagia using water swallowing test were 72% and 67%
respectively.123 The sensitivity of swallowing speed in detecting the swallowing dysfunction was
85.5%, and the specificity was 50%.122 The sensitivity of using choking or wet-horse voice as the
sole factor for predicting the presence of aspiration was 47.8%, while the specificity was
91.7%.122Some studies combined both water swallowing test and measurement of oxygen
desaturation using pulse oximetry to screen for dysphagia. The sensitivity and specificity were
found to range between 94.1% - 100% and 62.1% - 70.8% respectively.114-116
36
2.13 Effect of dysphagia on stroke outcome
Studies have shown that morbidity and mortality after acute stroke is increased if swallowing
problems are present even in patients with no reduction in level of consciousness.27, 59, 124-127 A
study showed that mortality in stroke patients with dysphagia was 37%.124 Another study
reported this to be as high as 42%.127 Conditions that result from swallowing difficulties in stroke
patient are aspiration pneumonia,19, 27, 59, 124 dehydration,59, 117 deterioration in nutritional status
and increase in length of hospital stay.27, 126. Aspiration pneumonia was particularly associated
with increased risk of both short-term and long-term mortality.53, 55, 56, 128 It was reported that
approximately 1 of 3 early deaths among stroke patients are related to pneumonia.53, 55
Aspiration pneumonia, which develops as a result of entrance of foreign materials into the
bronchial tree causing chemical pneumonitis with superimposed bacterial infection, is different
from hypostatic pneumonia which is one of the complications of prolonged bed rest. It usually
occurs in those with debilitated disease who remain recumbent in the same position for a long
period. The pneumonia results from infection developing in the dependent portion of the lung
due to decreased ventilation of these areas, with resulting failure to drain bronchial secretion.
2.14 Pseudodysphagia
Pseudodysphagia is the irrational fear of swallowing or choking. The symptoms are
psychosomatic in nature. The act of swallowing becomes mentally linked with choking. This can
37
induce panic reactions prior to or during the act of swallowing. Fear of choking is associated
with anxiety, depression, panic attacks, hypochondriasis, and weight loss.129 Pseudodysphagia is
essentially a diagnosis of exclusion. Another condition that could mimic pseudodysphagia is
Omohyoid Muscle Syndrome (OMS). Omohyoid muscle syndrome (OMS) is a rare clinical
condition that has the pathognomonic feature of the appearance of a lateral neck mass when
swallowing due to dysfunction of the omohyoid muscle. 129
Pseudodysphagia can also be described as a sensation of a lump in the throat--commonly known
as the globus symptom.130 Anxiety or psychological conflict is judged to be significantly related
to the onset and progression of the sensation. The sensation may lead to difficulty in swallowing
or breathing and may become severe or life threatening. The differential diagnosis is vast.131
_ENREF_88Statement of problem
Few studies have been done in our environment to look at the frequency of dysphagia and its
impact on outcome in acute stroke patients. There is high probability that the incidence of
dysphagia in acute stroke is under- reported in our environment. Screening patients with acute
stroke for dysphagia will go a long way in preventing aspiration pneumonia which is a major
complication of acute stroke. This will reduce morbidity and mortality associated with acute
stroke.
38
CHAPTER 3
METHODOLOGY
3.0 Study Site
This study was carried out at the Medical Wards and Accidents/ Emergency of the University
College Hospital (UCH), Ibadan, Oyo state. The University College Hospital, Ibadan, is a
foremost teaching hospital in Nigeria and receives patients referred from the whole country
especially South-Western Nigeria. The Neurology Unit of the hospital attends to stroke patients
presenting at the Emergency Room as well as those referred from other medical units.
3.1 Period of Study
Stroke patients were recruited consecutively as soon as they presented to UCH and each was
followed up for a period of one month. The study was conducted over nine months between
February 2013 and October 2013.
3.2 Study Design
The study was an observational prospective study involving stroke patients at UCH.
Bedside swallowing tests were carried out for all the stroke patients recruited and they were sub-
divided into those with dysphagia and those without.
39
3.3 SAMPLE SIZE DETERMINATION
N = 2 ( Zα + Z1-β)2 [P1 (1- P1) + P2 (1- P2)]
(P1 – P2)2
where,
N = minimum sample size for cases or controls
Zα = Standard normal deviate at 5% level of significance = 1.96
Z1-β = Standard normal deviate corresponding to a power of 80% = 0.84
P1 = Prevalence of dysphagia in patients with stroke = 56% 23
P2 = Prevalence of aspiration pneumonia in stroke patient with dysphagia = 20% 132
N = 2( 1.96 + 0.84)2 [ 0.56 (1-0.56) +0.2 ( 1- 0.2) ]
( 0.56 – 0.2)2
N = 49.1
The minimum sample size required was 49 each for the dysphagic and non-dysphagic. Hundred
patients each were recruited for the dysphagic and non-dysphagic in order to increase the power
of the study.
40
3.4 STUDY POPULATION
CASES
Inclusion criteria
Stroke patients aged 18 years and above
Patients with first- ever stroke
History and physical examination suggestive of stroke
Neuroimaging confirmation of a stroke (CT and / or MRI) or exclusion of any other cause for the
stroke presentation.
Exclusion criteria
Stroke onset >7days before assessment
Severely reduced conscious level (GCS ≤ 8). The GCS was checked repeatedly within 24 hours.
History of dysphagia before stroke.
Other neurological diseases or local pathology affecting swallowing.
Patient requiring continuous oxygen therapy or on mechanical ventilator.
Lack of consent to participate either from patients or relations on admission.
41
CONTROLS
Controls were stroke patients that did not have dysphagia on screening and had
the same inclusion and exclusion criteria as cases..
3.5 ETHICAL ISSUES
Ethical approval was obtained from Ethical Committee of UI/ UCH, Ibadan. A copy is
attached at the appendix.
The purpose of the study and its advantages were explained to all participants or relatives in the
language that they understood best. Thereafter, written informed consent was obtained from all
participants or relatives.
3.6 ASSESSMENT OF PARTICIPANTS
After written informed consent was obtained, a history and thorough basic neurological
examination was carried out on the patient. The history was obtained by directly questioning the
patient or a relative, or by referring to the case note in cases where the patient is aphasic and no
relative is present.
Using a questionnaire, demographic characteristics such as age, gender, place of residence,
ethnicity, marital status and socioeconomic status of the patient were obtained. Details of the past
medical history of the patient were enquired considering other conditions that could cause
dysphagia, risk factors for stroke, other co-morbidities and previous stroke. The social history of
the patient was obtained. National Institute of Health Stroke Scale (NIHSS) was used to
42
determine severity of stroke at admission. Glasgow Coma Scale (GCS) of the patient was
checked at admission. Patient’s functional outcome was assessed using Modified Rankin scale133
and Barthel index134 at presentation, after one week, two weeks and one month after stroke. A
copy of NIHSS, Modified Rankin Scale, and Barthel Index forms are attached at the appendix.
Assessment of dysphagia using Bedside Swallowing Tests were carried out at presentation, at
one week, two weeks, and a month after stroke.
3.6.1 Bedside Swallowing Tests
Gag Reflex: after explaining the test clearly to the patients, a sterile wooden tongue depressor
was used to touch the pharynx. Those patients that retched were considered to have positive gag
reflex. No patient vomited as a result of this test. This positive response suggested that the
patient could swallow.
.
Water Swallowing Test: After the test was clearly explained to the patients, they were seated
upright. 3mls of water was measured into a teaspoon and given to the patient to swallow. For
those patients who could not hold the teaspoon, they were helped to drink form it.59, 119 Those
patients who could swallow had the test repeated for them. The following signs of swallowing
difficulty were looked out for in each patient: coughing, choking after attempting to swallow,
water pooling in the mouth, delayed [>2 s] or absent swallow, poor or absent laryngeal elevation,
signs of distress or respiratory difficulty, and changed quality of phonation.
Afterwards, 10mls followed by 30mls and then by 50mls of water were measured into a
disposable cup. For those patients who could not hold the plastic cup, they were helped to drink
43
steadily form the container. Any patient that experienced any obvious difficulty in swallowing
during any of these tests was classified as having dysphagia. These tests were omitted in any
patient known to have choked on fluid that day and in those unconscious. Those Patients who
had depressed or absent gag reflex were tested initially with 3mls of water. Any patient who
choked was closely monitored and the managing team was advised to place the patient on nil per
oral. Oral hygiene was well maintained.19, 59, 113, 118, 123
Pulse oximetry: This measurement of peripheral oxygen saturation using pulse oximeter was
taken during the 10ml water-swallowing test. The oximeter probe was attached to the index
finger of the patient’s unaffected upper limb. Nail polish was removed from the finger, if there
was any, and they were instructed to keep that arm still during the study to avoid movement
artifact. The pulse oximeter was allowed to equilibrate for 5 minutes. A baseline measurement of
oxygen saturation was recorded. Oxygen saturation measurement was done continuously for 10
minutes from the start to allow time for the swallow assessment, any immediate or delayed
aspiration, and a recovery period. The oxygen saturation measurements were noted between 0 to
5 minutes (T1) and 5 to 10 minutes (T2) The greatest fall in oxygen saturation during the 2 time
periods from the onset of the water swallowing test (T1 and T2) were calculated as the difference
between the lowest saturation and the mean baseline saturation after excluding extreme values
due to movement or other artifacts.100, 111, 115 Oxygen desaturation ≥2% were considered to be
clinically significant.111,114-116
44
3.6.2 Treatment regime for stroke patients with dysphagia
Dysphagia is associated with aspiration and associated broncho-pulmonary infections, fluid
depletion and malnutrition. Dysphagia treatments may involve compensatory strategies which
include posture changes, heightening sensory input, swallow maneuvers (voluntary control of
selected aspects of the swallow), active exercise programs, diet modifications, non-oral feeding,
psychological support, or nursing intervention.135
Appropriate oral care was given to all the patients with dysphagia. Nasogastric (NG) tubes were
passed for all dysphagic stroke patients and blended meal, water and medications were given
through the NG tube. The tubes were replaced every two weeks or earlier if blockage occurred.
Enteral feeding was recommended for dysphagic stroke patients who could afford it.
Percutaneous endoscopic gastrostomy (PEG) was not done in this study. Although use of PEG
tubes are less irritating and may not require replacement for months, the procedure is invasive,
requiring sedation and endoscopy, and has a number of potential complications.136, 137
3.6.3 Presence of aspiration pneumonia was diagnosed based on the presence of ≥3 of the
following variables: fever (38°C), abnormal respiratory examination (tachypnea [>22/min],
inspiratory crackles, bronchial breathing), tachycardia, abnormal chest radiograph, arterial
hypoxemia (PO2 <70 mm Hg), and isolation of a relevant pathogen (positive gram stain and
culture) and leukocytosis.124, 132, 138 Those patients who had aspiration pneumonia were treated
with antibiotic based on organism sensitivity test.
45
3.6.4 Neuroimaging studies
A computerized tomography (CT) scan of the brain was done for all of the patients to ascertain
the stroke type, lesion site, and lesion size. CT early signs of ischaemia that were looked for were
hypodensity of brain tissue, poor grey-white matter differentiation, obscuration of lentiform
nucleus (blurred basal ganglia), blurring of insular ribbon, and hyperdense middle cerebral artery
(MCA). Haemorrhagic stroke appears as hyperdense lesion on brain CT scan.1, 43, 49
Measurement of haematoma volume was calculated using maximum length, crossed short length,
slice thickness.139 Lesion size of acute cerebral infarction was derived from the area of the lesion
and slice thickness. The area of abnormal low attenuation was traced on each CT slice, and the
area was summed for the slices showing the infarct.140
3.6.5 Laboratory evaluation
Blood samples for Full Blood Count, Serum Electrolytes and Urea, Random Blood Glucose and
Lipid profiles were obtained from each patient. Chest radiograph was done for all the patients.
46
Operational definitions
Dysphagia; acute stroke patients that had negative 10ml water swallowing test and
peripheral oxygen desaturation ≥2% were considered to have dysphagia.114-116
Computerized tomography (CT) definition of stroke type: presence of hyperdensity on
non-contrast CT (NCCT) brain scan in acute stroke patient is hemorrhagic stroke.
Presence of hypodensity or hypo-attenuation on NCCT brain scan in acute stroke patient
defines ischemic stroke.
CT definition of ischemic stroke subtype (OCSP):45
Total anterior circulation infarct (TACI): large anterior circulation infarcts with both
cortical and subcortical involvement.
Partial anterior circulation infarct (PACI): predominantly cortical infarcts.
Posterior circulation infarct (POCI): infarcts clearly associated with the vertebrobasilar
arterial territory.
Lacunar infarct (LACI): infarcts confined to the territory of the deep perforating arteries.
Limitation of the Study
Inability of all patients with stroke to have neuroimaging done due to cost of the imaging
excluded many patients from being recruited and prolonged the time required to achieve the
required number of subjects.
47
DATA COLLECTION AND ANALYSIS
Information was obtained from the eligible patients using a questionnaire. Data collection was
commenced after an informed consent was obtained from the patient or the relatives of the
patient and after ethical approval.
All patients’ socio-demographic and clinical characteristics data were presented in tables and
charts using summary statistics of proportions for categorical variables and means± standard
deviation for normally distributed continuous variables. The non-parametric variables were
presented using median. The Chi-square or its equivalent was used to compare proportions while
student t-test or its non-parametric equivalent where appropriate, was used to compare
continuous variables. The level of statistical significance was set at p- value of <0.05.
Multivariate logistic regression models were constructed to assess for independent predictors of
dysphagia in acute stroke patients with variable that showed significant statistical association
with dysphagia both in the study and from literature fitted into the model..
Repeated measures ANOVA was carried out to assess the impact of dysphagia and aspiration on
clinical outcome as measured by the Modified Rankin Scale and Barthel Index. Also, survival
analysis was done to assess the impact of dysphagia and aspiration on mortality, with Kaplan-
Meier curves constructed and Log rank test performed to assess for statistically significance
difference. Cox proportional hazard model was used to assess possible causes of death in the
patients with dysphagia.
.All data was analyzed using Statistical Package for Social Sciences (SPSS) version 16.
48
CHAPTER FOUR
RESULTS
Four hundred stroke patients presented to UCH during the 9-month study period. Out of the 200
patients that fulfilled the inclusion criteria, ninety nine (99) patients had dysphagia and were
recruited as cases while one hundred and one (101) patients who did not have dysphagia were
recruited as controls. Reasons for exclusion included inability to do neuroimaging (n=111), pre-
hospital delay of more than 7 days (n= 16), repeat stroke (n= 15), GCS less than 8 (n= 35),
patient on mechanical ventilator (n= 15), and refusal of the relations to give informed consent
(n= 8).
Socio-demographic characteristics of the study population
The dysphagic stroke patients comprised 52 (52.5%) male and 47 (47.5%) female while non-
dysphagic stroke consisted of 52 (51.5%) male and 49 (48.5%) female (p= 0.88). The mean ages
for the non-dysphagic and dysphagic stroke were 59.5±11.5 years and 62.1±12.1 years
respectively (p= 0.11). The participants were well matched for age and sex as there
was no statistically significant difference in age and sex when the values were
compared between the dysphagic and non-dysphagic stroke groups. All non-
dysphagic stroke group and 97 (97.98%) of dysphagic stroke were right handed. (p= 0.15).
49
Figure 1: Comparison of gender distribution in dysphagic and non-dysphagic stroke
patients
52.5%
51.5%
47.5%
48.5%
44.00%
45.00%
46.00%
47.00%
48.00%
49.00%
50.00%
51.00%
52.00%
53.00%
Cases Controls
Male
Female
50
Clinical characteristics of the study population
In this study, hypertension was the most common risk factor for stroke identified in both
dysphagic 99 (100%) and non-dysphagic stroke 98 (97.07%). However, there was no statistically
significant difference between the two groups (p=0.08).
Diabetes mellitus was not as common as hypertension as a risk factor for stroke in both
dysphagic and non-dysphagic stroke in this study. More non-dysphagic stroke group 19
(18.81%) had diabetes mellitus than the dysphagic stroke 15 (15.15%). However, it was not
statistically significant. (p=0.49)
The observed difference in GCS at presentation between dysphagic and non-dysphagic was
statistically significant (p <0.01). The patients with dysphagia had significantly worse GCS at
presentation than the non-dysphagic group as shown in Table 1.
NIHSS of dysphagic stroke patients at presentation (22.81±6.23) was significantly higher than
the non-dysphagic group (8.92±6.37). The observed difference was statistically significant (p
<0.01). (Table 1)
TABLE 1: Comparison of GCS and NIHSS of study participants.
Variable Dysphagic Non-dysphagic P-value
GCS at presentation
14-15
9-13
16 (16.16%)
83 (83.84%)
83 (82.18%)
18 (17.82%)
<0.01
NIHSS±SD 22.81±6.23 8.92±6.37 <0.01
. GCS- Glasgow Coma Score. NIHSS: National Institute of Health Stroke Scale.
51
.
The mean pulse rate (p<0.00), systolic blood pressure (p=0.01) and diastolic blood pressure
(p=0.03) were significantly higher in dysphagic stroke than in non-dysphagic stroke patients
as shown in table 2 below.
TABLE 2: Clinical Characteristics of the Study Population
Variables Dysphagic Non-dysphagic P-value
Pulse rate ±SD 93.92± 17.39 86.16 ±12.51 <0.00
Systolic Blood Pressure ±SD 189.67 (38.80) 174.18 (36.77) 0.01
Diastolic Blood Pressure ±SD 109.25 (23.16) 102.35 (20.66) 0.03
Mean arterial pressure 136.10 `126.29 0.04
52
Table 3 shows comparison of laboratory parameters between dysphagic and non-dysphagic
stroke patients. The mean random blood sugar observed was significantly higher in dysphagic
(167.19±92.26) than non-dysphagic (141.17±57.22). p=0.033.
Dyslipidemia with high total Cholesterol and high LDL-C were observed in both dysphagic and
non-dysphagic stroke patients. However, there was no significant statistical difference in the
levels of lipid profiles between the dysphagic and non-dysphagic groups as shown in Table 3 (p=
values 0.834, 0.065, 0.161, 0.062).
Table 3: Comparison of laboratory parameters between Cases and Controls
Variables Dysphagic (99) Non-dysphagic (101) P-values
RBS at admission (Mg/dL)±SD 167.19±92.26 141.17±57.22 0.033
Lipids Value (Mg/dL)
Total Cholesterol ±SD
Triglyceride ±SD
HDL-C ±SD
LDL-C ±SD
211.8±64.45
128.7±48.57
55.6±21.74
121.4±45.2
208.4±50.08
105.4±39.45
51.0±14.37
134.8±40.29
0.834
0.065
0.161
0.062
53
Table 4 below shows frequency of dysphagia among 200 stroke patients that fulfilled all the
inclusion criteria. Using gag reflex method only, the frequency was 99 (49.50%). With 3ml WST
only, the frequency was 95 (47.48%). With 10mls WST only, it was 97 (48.50%), and Using
Peripheral Oxygen desaturation method, the frequency was 93 (46.47%). 95% confidence
interval of each method was as stated in table 4.
TABLE 4: Frequency of dysphagia among stroke admissions during study period.
Variables Frequency Percentage 95% CI
Gag Reflex 99 49.50 43.19 – 54.58
3ml WST 95 47.48 42.49 – 53.59
10ml WST 97 48.50 43.49 – 53.59
Peripheral Oxygen
desaturation
93 46.47 41.99 – 53.47
WST: Water Swallowing Test. CI: Confidence Interval
54
More non-dysphagic stroke {65 (64.36%)} than dysphagic stroke patients {35 (35.35%)} had
ischaemic stroke while more dysphagic {64 (64.65%)} than non-dysphagic {36 (35.64%)} had
haemorrhagic stroke. These differences were statistically significant, p<0.001. (Table 5).
TABLE 5: Distribution of stroke types in dysphagic and non-dysphagic stroke patients.
Variables Dysphagic (%) Non-dysphagic (%) P-value
Ischaemic
Haemorrhagic
35 (35.35%)
64 (64.65%)
65 (64.36%)
36 (35.64%)
<0.001
Total 99 101
55
Table 6 shows classification of cerebral infarct based on Oxfordshire Community Stroke Project
(OCSP) classification. Four of dysphagic (11.4%) and two of non-dysphagic (3.1%) had TACI.
This was not statistically significant (p= 0.393). 55 of non-dysphagic (84.6%) and 26 of
dysphagic (74.3%) had PACI and this difference was statistically significant (p= 0.001). Four of
dysphagic (11.4%) and two of non-dysphagic (3.1%) had POCI (p=0.092). 2.9% of dysphagic
and 9.2% of non-dysphagic had lacunar syndrome (p= 0.620)
Table 6: Distribution of vascular territories involved in dysphagic and non-dysphagic
ischaemic strokes.
Variable Cases (%)
(35)
Controls (%)
(65)
P- value
TACI 4 (11.4%) 2 (3.1%) 0.393
PACI 26 (74.3%) 55 (84.6%) 0.001*
POCI 4 (11.4%) 2 (3.1%) 0.092
Lacunar syndrome 1 (2.9%) 6 (9.2%) 0.620
TACI: Total anterior circulation infarct. PACI: Partial anterior circulation infarct . POCI: Posterior circulation .
infarct.
56
Table 7 shows sites of stroke lesion in dysphagic and non-dysphagic stroke patients. Fifty-one of
dysphagic stroke patients (49.5%) and fifty-two of non-dysphagic stroke patients (50.5%) had
cortical lesions. This difference was not statistically significant (p =1.00). Subcortical
involvement of stroke was more in dysphagic stroke than in non-dysphagic stroke patients.
Sixty-four of dysphagic stroke patients (57.1%) and 48 of non-dysphagic stroke patients (42.9%)
had lesion at subcortical regions. This difference was statistically significant (p =0.015). Six of
dysphagic stroke patients and three of non-dysphagic stroke had stroke lesion at
brainstem/cerebellar sites. This difference was not statistically significant (p=0.29).
Sixteen of dysphagic stroke and 2 of non dysphagic stroke patients had both cortical and sub-
cortical lesions
TABLE 7: Stroke lesion sites in study participants.
Lesion site Dysphagic Non-dysphagic P- value
Dominant hemisphere
53 (53.5%)
52 (51.5%)
0.775
Non-dominant hemisphere
46 (46.5%)
49 (48.5%)
0.839
Total 99 101
Cortical n=103(%)
51(49.5%)
52(50.5%)
1.00
Sub-cortical n=112(%)*
64(57.1%)
48(42.9%)
0.015
Brainstem/Cerebellum n=9(%)
6(66.7%)
3(33.3%)
0.29 16 cases and 2 controls had both cortical and sub-cortical lesions
57
.Table 8 below shows complications observed in dysphagic and non-dysphagic stroke patients.
The commonest complication observed in the dysphagic was aspiration pneumonia. Sixty two of
the dysphagic (62.63%) and one of the non-dysphagic (0.99%) had aspiration pneumonia. Same
number of dysphagic and non-dysphagic had urinary tract infection (UTI). UTI was the
commonest complication observed in the non-dysphagic. Eight of the controls (7.92%) and ten
of the dysphagic (10.10%) had biochemical features of renal impairment. However, the
difference was not statistically significant (p=0.590). Three of the non-dysphagic (2.97%) and
two of the dysphagic (2.04%) had deep venous thrombosis. The difference was not statistically
significant (p= 0.327). One of the dysphagic (1.02%) and three of the non-dysphagic (2.97%)
had pulmonary thromboembolism. This was not statistically significant (p=0.675). None of the
dysphagic had myocardial infarction as complication while one of the non-dysphagic (0.99%)
had it.
TABLE 8: Frequency of complications observed in study participants.
Variable Dysphagic (%) Non-dysphagic (%) P-value
Urinary tract infection 20 (20.20%) 20 (19.80%) 0.944
Acute kidney injury 10 (10.10%) 8 (7.92%) 0.590
Pulmonary thromboembolism 1 (1.02%) 3 (2.97%) 0.675
Deep venous thrombosis 2 (2.04%) 3 (2.97%) 0.327
Myocardial infarction 0 (0.00%) 1 (0.99%) 0.321
Aspiration Pneumonia 62 (62.63%) 1 (0.99%) <0.001*
58
Table 9 below shows patients’ outcome in dysphagic and non-dysphagic. Seventy nine of
dysphagic (79.80%) and sixteen of non-dysphagic (15.84%) died on admission. The difference
was statistically significant (p< 0.001). The average survival days for the non-dysphagic were
24.56 days and for dysphagic were 12.21 days. The difference was also statistically significant
(p< 0.001).
TABLE 9: Outcome of dysphagic and non-dysphagic stroke patients.
Variable Dysphagic Non-dysphagic P-value
Died On Admission 79 (79.80%) 16 (15.84%) <0.001
Survival Time (Days) 12.21 (±1.15) 24.56 (±1.19 ) <0.001
.
59
Kaplan Meier survival curve in figure 2 below clearly depicts percentage cumulative survival in
the dysphagic and non-dysphagic. Those with dysphagia were on admission for a longer period
in the hospital and some of them died.
Figure 2: Kaplan-Meier survival curve for cases and control.
60
Table 10 below compares outcome of patients that had dysphagia alone with patients that had
dysphagia complicated by aspiration pneumonia. The outcome was worse with the dysphagic
that had aspiration pneumonia. 55 of patients (69.6%) that had dysphagia complicated by
aspiration pneumonia died on admission. 24 of the patients (30.4%) that had dysphagia without
aspiration died on admission. The difference was statistically significant (p= 0.004). 30-day case
fatality rate for patient with dysphagia alone was 24.2%. 30-day case fatality rate for dysphagic
stroke patients complicated with aspiration pneumonia was 55.6%. The average survival days in
the patients with dysphagia alone was shorter in dysphagic complicated by aspiration pneumonia
(p= 0.023) than in non-dysphagic.
TABLE 10: Outcome of patients with dysphagia alone and patients with dysphagia and
aspiration pneumonia.
Variable Dysphagia Alone Dysphagia with Aspiration P-value
Died On Admission 24 (30.4%) 55 (69.6%) 0.004
Survival Time (Days) 14.97 (±4.08) 9.53 (±0.88) 0.023
61
Kaplan Meier survival curve in figure 5 clearly depicts percentage cumulative survival in the
dysphagic without aspiration and those with aspiration. The survival drastically reduced in those
patients that had aspiration pneumonia.
Figure 3: Kaplan-Meier survival curve for patient with dysphagia without aspiration and
those with aspiration
62
Table 11 below shows outcome in dysphagic and non-dysphagic using Modified Rankin Scale
(MRS). The mean MRS of the dysphagic stroke patients at 4th week post stroke was 3.83 (SD±
1.029). The mean MRS of non-dysphagic stroke patients at 4th week was 2.55 (SD± 1.34). This
difference was statistically significant. (p< 0.001). The mean BI of dysphagic stroke patients at
4th week post stroke was 28.04 (SD± 32.15) while the mean BI of non-dysphagic stroke patients
was 65.52 (SD± 30.33). This difference was also statistically significant.(p< 0.001).
TABLE 11: Outcome of dysphagic and non-dysphagic stroke patients using Modified
Rankin Scale (MRS) and Barthel Index (BI)
Variable Dysphagic Non-dysphagic P-value
MRS at 4th week ±SD 3.83 ± 1.029 2.55 ± 1.34 <0.001
BI at 4th week ±SD 28.04± 32.15 65.52 ± 30.33 <0.001
63
Table 12 below compares MRS at 4th week in stroke patients that had dysphagia complicated by
aspiration pneumonia to those that had dysphagia alone. The mean MRS of dysphagic stroke
patents that had aspiration pneumonia at 4th week was 4.38 (SD± 0.52) while the mean MRS of
dysphagic stroke patients without aspiration pneumonia at 4th week was 3.53 (SD± 1.13). This
difference was not statistically significant (p=0.142). The mean BI of dysphagic stroke patients
that had aspiration pneumonia at 4th week post stroke was 18.75 (SD± 24.31) while the mean BI
of dysphagic stroke patients without aspiration pneumonia at 4th week post stroke was 33.00
(SD± 35.39). This difference was not statistically significant. (p=0.209).
TABLE 12: comparison of outcome of stroke patients with dysphagia alone and outcome of
stroke patients with dysphagia complicated by aspiration pneumonia using Modified
Rankin Scale (MRS) and Barthel Index (BI)
Variable Dysphagia with aspiration Dysphagia alone P-value
MRS at 4th weeks ±SD 4.38 ± 0.52 3.53 ± 1.13 0.142
BI at 4th week ±SD 18.75 ± 24.31 33.00±35.39 0.209
64
Table 13 shows univariate and multivariate logistic regression analysis to assess determinants of
30-day case fatality in this study. Determinants of 30-day case fatality with statistical
significance were dysphagia (p <0.001), aspiration pneumonia (p <0.001), sepsis (p <0.001),
severe NIHSS (p <0.001), haemorrhagic stroke subtype (p <0.001), and mean arterial pressure
(MAP) >145mmHg (p =0.041). With multivariate analysis, the most significant determinant of
30-day case fatality in this study was dysphagia (p= 0.005). This was followed by aspiration
pneumonia (p =0.024), haemorrhagic stroke (p= 0.043) and severe NIHSS (0.049).
Table 13: Univariate and Multivariate Binary logistic regression analysis to assess the
determinants of 30- day case fatality.
Variables
Analysis
Univariate
OR(95% CI)
p-value Multivariate
Β (95% CI)
p-value
Dysphagia
Yes
No
1(reference - death)
0.20 (0.13-0.32)
<0.001
0.29(0.08-0.63)
0.005
Aspiration Pneumonia
Yes
No
1(reference- death)
0.29(0.22-0.40)
<0.001
0.28(0.09-0.84)
0.024
Sepsis
Yes
No
1(reference- death)
0.23(0.11-0.50)
<0.001
0.42(0.14-1.23)
0.112
NIHSS
Severe (21-42)
Mild-Moderate(0-20)
1(reference- death)
0.31(0.22-0.42)
<0.001
0.36(0.13-1.00)
0.049
Gender
Male
Female
1(reference-death)
0.79(0.56-1.06)
0.112
NA
Stroke Subtype
Ischaemic
Haemorrhagic
1(reference-death)
2.18(1.55-3.02)
<0.001
2.34(1.03-5.31)
0.043
Post Stroke
Hyperglycaemia
RBS > 140
RBS <140
1(reference-death)
0.76(0.55-1.04)
0.092
NA
Mean Arterial Pressure
MAP> 145
MAP<145
1(reference-death)
0.72(0.54-0.97)
0.041
1.05(0.40-2.72)
0.923
NA- Not analysed
65
Table 14 below shows Cox Proportional hazard model after controlling for the effect of sepsis in
those patients that aspirated. Hazard ratio (HR) of aspiration among those without sepsis was
2.883 (p= 0.036) and this was statistically significant. Hazard ratio of aspiration complicated by
sepsis was 1.525 and was not statistically significant (p= 0.335)
Table 14: COX Proportional Hazard Model for Patients with Dysphagia controlling for the
effect of sepsis
Variable Beta SE p-value HR 95% CI
Aspiration without sepsis 1.059 0.509 0.036 2.883 1.070 – 7.767
Aspiration with Sepsis 0.422 0.438 0.335 1.525 0.646 – 3.600
*P-value <0.05- significant SE: Standard Error. HR: Hazard ratio. CI: Confidence Interval.
66
CHAPTER FIVE
DISCUSSION
Dysphagia following acute stroke is a common and serious problem. It is being increasingly
recognized now that unilateral hemispheric affectation can cause dysphagia.18, 62, 72, 141
Socio-demographic characteristic of the study population
The mean age of subjects at presentation was 60.8± 11.8 years. This finding is similar to reports
by Danesi et al in urban Nigeria where the mean age at presentation was 58.5±13.5 years.41
Other studies done in Nigeria showed almost similar ages at presentation.40, 142, 143 However,
these mean ages were found to be lower than the findings of Osuntokun where the ages at
presentation were 8th decade in male and 7th decade in female.5 The difference in the peak ages at
onset of stroke is probably due to increased incidence of cardiovascular risk factors for stroke
among the middle aged group. Study by Owolabi et al144 showed that stroke in the young adult
was not as uncommon as was previously suggested. The cardiovascular risk factors identified in
that study were hypertension, hypercholesterolemia, and diabetes mellitus.144 The fact that
middle aged group is now mostly affected by stroke will have significant economic, social and
medical burden on low resource countries including Nigeria.
This study also showed male to female (M: F) ratio of 1.08: 1.0. This was similar to findings by
Remesso, et al74 in 2011 where the M: F was 1.02:1. Male to female ratios found by Danesi41 and
67
Obiakor16 were 1.45:1 and 3.1:1 respectively. Desalu40 and Onwuchewa143 found a slightly
higher female to male ratio. Findings from all these studies showed a clear departure from
previous impression that stroke was much commoner in male. The role of risk factors unique to
women such as the use of oral contraceptives, hormone replacement therapy, pregnancy, and
insufficient treatment of conventional stroke risk factors in women have all been considered as
probable explanations.145
Clinical characteristics of study population
The commonest risk factor for stroke found in this study in both dysphagic and non-dysphagic
stroke patients was hypertension. This finding was consistent with other findings in Nigeria5, 38,
40, 42, 142, 146, 147 and in Sub-Saharan Africa.33, 34, 148, 149 Other risk factors identified were diabetes
mellitus and dyslipidemia. Africa bears a heavy burden of stroke. In order to stem the surge of
stroke and other vascular diseases in Nigeria and in Sub-Saharan Africa at large, a better
coordinated community-based primary and secondary prevention programs needs to be
instituted. This will help in curtailing these cardiovascular risk factors for stroke.
National institute health stroke scale (NIHSS) score of study participants was significantly higher
at presentation in dysphagic stroke patients than in non-dysphagic. The average NIHSS of the
dysphagic was in severe category and this also affected the outcome of the dysphagic stroke
patients as it contributed significantly to the 30-day case fatality. Dawodu,150 Adams et al,151 and
Fonarow et al152 showed that initial NIHSS score predicted mortality risk in stroke patients. The
68
mean initial NIHSS score in stroke patients with complications was much higher than those
without complication.
Frequency of dysphagia among stroke patients.
The frequency of dysphagia in this study was 46.47% with peripheral oxygen desaturation and
48.50% with 10mls water swallowing test. These findings were similar to results from other
studies that used similar methods.72, 106, 116, 132, 153-155 The incidence of dysphagia in stroke
patients ranged from 65% to 81% when Videofluoroscopy and FEES, the gold standards for
detecting dysphagia, were used.76, 87, 156 Positive and negative predictive values of the bedside
swallowing methods used in this study were not estimated as the gold standards for detecting
dysphagia (Videofluoroscopy and FEES) were not available.
This study showed that checking for gag reflex is a useful method for screening for dysphagia in
stroke patients. 49.50% of those patients screened were found to have absent gag reflex (95% CI:
43.19-54.58). This finding was consistent with other studies which showed that absent gag reflex
is predictive of aspiration in stroke patients.106-108 However, findings of some other studies
showed that using gag reflex alone to screen for dysphagia in stroke patients had low sensitivity
and specificity.110, 123, 157, 158 It was found in other studies that Peripheral Oxygen desaturation
during swallowing of 10mls of water had high specificity.111, 114, 115 Studies have shown that
combination of both water swallowing test (WST) and peripheral oxygen desaturation method
increased sensitivity and specificity of detecting dysphagia in stroke patients.20, 115, 116, 157 These
findings from this study underscored the importance of checking for swallowing difficulty in all
stroke patients.
69
Brain lesion and occurrence of dysphagia
It was observed in this study that 64.65% of patients with dysphagia had hemorrhagic stroke
(p<0.001) while the predominant stroke type in those patients without dysphagia was ischemic
(64.36%) (p< 0.001). These findings were statistically significant. These findings are similar to
the findings of Paciaroni et al159, Sundar et al141 and El-Sheikh W. M155 where it was noted that
dysphagia was more frequent in patients with hemorrhagic stroke. Remesso et al64 also noted that
severity of dysphagia was worse in patients with hemorrhagic stroke. Although hemorrhagic
stroke is less common than ischemic stroke, presence of hemorrhagic stroke may be predictive of
swallowing dysfunction.
This study also showed that the laterality of neurological deficit appeared not to influence the
development of dysphagia. All the controls and almost all the cases were right-handed, inferring
left hemispheric dominance. 53.5% of patients with dominant hemispheric lesion and 46.5% of
patients with non-dominant hemispheric lesion developed dysphagia. In those patients without
swallowing dysfunction, 51.5% had dominant hemispheric lesion while 48.5% had non-
dominant hemispheric lesion. These differences were not statistically significant. These findings
were comparable to findings in other studies.141, 155, 159, 160 It is becoming increasingly evident
that unilateral affectation of either lobe, dominant or non-dominant, can result in dysphagia
contrary to the earlier belief that only bi-hemispheric lesions, where supratentorial structures are
concerned, could lead to dysphagia.62, 66 Studies by Hamdy et al63, 72 suggest that swallowing is
represented bilaterally but asymmetrically with no clear right or left laterality and the size of the
cortical area associated with swallowing in the unaffected cortex determines the presence or
absence of dysphagia. We can therefore infer that there is the possibility of unilateral
70
hemispheric dominance which varies between individuals. Further studies requiring serial
imaging and transcranial magnetic stimulation to identify the swallow-dominant side can help
determine whether there is a dominant hemisphere in each individual that, if affected, results in
swallowing dysfunction or if the increased representation of swallowing in the unaffected
hemisphere is a result of cortical reorganization and compensation.
Only six study participants had TACI based on Oxfordshire Community Stroke Project (OCSP)
classification of cerebral infarct. Four of the patients with TACI had dysphagia and the other two
did not have it. Although this finding was not statistically significant (p= 0.393) probably due to
the small number of patients that had TACI, Sundar et al141 in his study found that all the
patients that had TACI had swallowing difficulty. Presence of dysphagia in TACI is probably
due to large area of hemispheric infarction involved. Only one out of the seven patients in the
study population that had lacunar syndrome had dysphagia. This finding is consistent with the
findings of Sundar141 and Ellul et al.161 The fact that patients with lacunar stroke has lower
incidence of dysphagia may probably be due to smaller infarct volume and better collateral
circulation through the Circle of Willis.
Although supplementary motor area, represented in the superior and middle frontal gyri, is
believed to be associated with planning of sequential movements, as occurs with swallowing88
lesions in the cortical areas were not significantly associated with dysphagia in this study. This
was similar to the findings of Gonzalez-Fernandez et al.98 Findings from this study showed that
sub-cortical lesions were associated with swallowing. This was similar to the findings in other
studies.91, 98 The later stages of swallowing process are largely involuntary and are controlled by
71
subcortical mechanisms which may be affected by basal ganglia, thalamic, large hemispheric or
bi-hemispheric lesions.162 Subcortical lesions found to be associated with dysphagia in this study
involved the internal capsule, thalamus and basal ganglia..
Brainstem/ cerebellar lesions were found more in dysphagic than in non-dysphagic stroke
patients in this study. The difference was not statistically significant probably due to small
numbers of patients with brainstem and cerebellar lesions. Lesions in brainstem were found in
several other studies to be associated with dysphagia.64, 141, 155, 163, 164 Dysphagia is common in
brain stem strokes probably due to lower motor involvement of bulbar swallowing mechanisms.
Lesions in the brainstem could affect the sensitivity of the oral cavity, tongue and cheeks, and
could trigger swallowing disorders and laryngeal elevation.60, 77
.
Stroke severity and dysphagia
The initial mean National institute health stroke scale (NIHSS) score was higher in dysphagic
stroke patients than in non-dysphagic stroke. The initial mean NIHSS of dysphagic and non-
dysphagic stroke patients was 22.81±6.23 and 8.92±6.37 respectively. This difference was
statistically significant. Jevaseelan et al166 showed that NIHSS >9 was moderately predictive of
clinically relevant dysphagia. Okubo et al167 also showed that NIHSS is highly sensitive and
specific in detecting dysphagia, with NIHSS score of 12 being suggested as a cutoff value.
Beside the fact that high NIHSS score contributed to the 30-day mortality in this study, it appears
there is an association between initial NIHSS score and presence of dysphagia.
72
Effect of dysphagia on the 30-day outcome in acute stroke patients.
This study clearly showed that swallowing difficulty contributed significantly to the morbidity
and mortality of acute stroke patients. 79.8% of acute stroke patients with dysphagia died on
admission while 16.8% of group of patients without dysphagia died. This study also showed that
stroke patients without dysphagia survived significantly longer (25.56 days) than those with
dysphagia (12.21days). 30-day case fatality rate for patient with dysphagia alone was 24.2%.
Modified Rankin Scale (MRS) and Barthel Index (BI) were used in this study to objectively
measure the functional outcome of dysphagic stroke patients and non-dysphagic stroke patients.
The findings were statistically significant. Findings from this study showed that stroke patients
with dysphagia had worse functional outcome at the end of 4th week based on the MRS and BI
values. These findings were comparable to results of other studies.19, 52-54, 56, 128, 155, 169, 170 Study
by Remesso et al showed that stroke patients who showed abnormalities of swallowing had
higher mortality rates.64 Smithard et al124 concluded that the presence of dysphagia was
associated with an increased risk of death, disability, length of hospital stay, and institutional
care among stroke patients. Study by Paciaroni.et al159 revealed that stroke mortality and
disability were independently associated with dysphagia.
Apart from respiratory complication that is associated with dysphagia, dehydration and
deterioration in nutritional status have also been found to be common complications of
73
dysphagia.27, 59, 117, 126 Parameters for assessing dehydration and deterioration in nutritional status
were not checked for in this study.
Frequency of aspiration pneumonia in acute stroke patients with dysphagia.
There is high incidence of dysphagia after stroke which is also associated with increased risk of
aspiration pneumonia. Dysphagia is an independent risk factor for aspiration in patients with
acute stroke.62, 168
In this study, presence of aspiration pneumonia in stroke patients with dysphagia was diagnosed
based on the presence of ≥3 of the following clinical variables: fever (>38°C), Abnormal
respiratory examination (Tachypnea (>22/min), Chest crackles and bronchial breathing),
tachycardia, CXR abnormality, and Leucocytosis. These criteria were also used in other studies
to diagnose aspiration pneumonia.132, 141, 155
The frequency of aspiration pneumonia in those patients with dysphagia in this study was 62.6%.
Aspiration pneumonia was also the commonest complication of acute stroke found in this study.
This was similar to findings of Obiako et al in 2011.16 Other studies also showed that aspiration
pneumonia was the commonest complication in stroke patients that had swallowing
dysfunction.52, 55, 56, 128, 155
These findings further highlight the importance of screening for dysphagia in acute stroke
patients in other to prevent complication of aspiration pneumonia which may increase morbidity
and mortality in stroke.
74
Effect of aspiration pneumonia on the 30-day outcome in acute stroke patients
This study showed that aspiration pneumonia contributed significantly to the morbidity and
mortality of acute stroke patients. More patients with aspiration pneumonia died (69.4%) on
admission compared to 30.4% of dysphagic patients without aspiration that died on admission.
Also, patients that had aspiration pneumonia survived for much shorter days (9.5 days) than
those patients without aspiration (15 days). These findings were statistically significant. This
study also showed that dysphagic stroke patients that had aspiration pneumonia had worse
functional outcome based on the MRS and BI at 4th week post stroke than those without
aspiration pneumonia. 30-day case fatality rate for dysphagic stroke patients complicated by
aspiration pneumonia was 55.6%. These findings were comparable to results of other studies. In
a large community-wide study of stroke outcomes by Katzan et al55, pneumonia conferred a
threefold increased risk of 30-day death. Aslanyan et al128 showed that pneumonia was
associated with poor outcome in acute stroke patients. Heuschmann et al53 did a study on
predictors of in-hospital mortality and attributable risks of death after ischemic stroke. Aspiration
pneumonia was the complication with the highest attributable proportion of death in the entire
stroke population. Vermeij et al56 concluded that stroke-associated infection, in particular
pneumonia, was independently associated with poor functional outcome after stroke.
75
Logistic regression was used to determine variables associated with 30-day stroke fatality in this
study. Variables considered were dysphagia, aspiration pneumonia, baseline NIHSS, gender,
sepsis, stroke subtype, post stroke hyperglycemia, and mean arterial pressure at presentation.
In the multivariable analysis, dysphagia, aspiration pneumonia, severe baseline NIHSS, and
haemorrhagic stroke subtype were important determinants of 30-day case fatality.
When a regression analysis was done for the stroke patients with dysphagia, aspiration was
found to be an independent predictor for death. On further analysis, after controlling for the
effect of sepsis on those patients that aspirated, the Hazard Ratio (HR) of aspiration among those
without sepsis was statistically significant.
76
CHAPTER SIX
CONCLUSION
The frequency of dysphagia in this study was 46.47% with peripheral oxygen desaturation and
48.50% with 10mls water swallowing test.
Haemorrhagic stroke type was associated with dysphagia in acute stroke patients in this study. .
Stroke lesions in the subcortical regions were more associated with dysphagia than cortical
lesions. There was an association between stroke severity and dysphagia. The size of stroke
lesion was also associated with dysphagia. Stroke patients with large lesion sizes had increased
propensity to develop dysphagia.
Dysphagia contributed significantly to the morbidity and mortality of acute stroke patients in this
study. 78.9% of stroke patients with dysphagia died on admission with their average survival
days shorter than those without swallowing difficulty. Dysphagic stroke patients had worse
functional outcome at the end of 4th week based on the MRS and BI values. 30-day case fatality
rate for patient with dysphagia alone was 24.2%.
The frequency of aspiration pneumonia in stroke patients with dysphagia in this study was
62.6%. Aspiration pneumonia contributed significantly to the morbidity and mortality of acute
stroke patients in this study. 69.4% of patients with aspiration pneumonia died on admission with
77
the average survival days much shorter than those without aspiration pneumonia. Functional
outcome based on MRS and BI values at 4th week was worse in patients with aspiration
pneumonia. 30-day case fatality rate for dysphagic stroke patients complicated by aspiration
pneumonia was 55.6%.
In the multivariable regression analysis, dysphagia, aspiration pneumonia, severe baseline
NIHSS, and haemorrhagic stroke subtype were important determinants of 30-day case fatality in
this study.
78
RECOMMENDATION
Based on the outcome of this study, the following are recommended:
1. Use of simple bedside swallowing tests as effective screening tool in detecting dysphagia
in all stroke patients.
2. Stroke patients with identified risk factor for aspiration should be monitored for infection.
3. To improve long-term survival of stroke patients, aggressive management of pulmonary
complication should be instituted early.
4. If dysphagia is recognized early, chest infection may be prevented with the use of
nasogastric tubes, parenteral nutrition, or percutaneous endoscopy gastrostomy until
swallowing recovers.
5. Chest physiotherapy plays an important role in the management of stroke patient with
aspiration pneumonia.
6. Further studies are required to find out if stroke patients with dysphagia will benefit from
prophylactic antibiotic treatment.
79
LIMITATIONS
1. Inability to use instrumental investigation of swallowing impairment, such as
Videofluoroscopy and Fiberoptic Endoscopic Evaluation of Swallowing (FEES), which
are gold standards for detecting dysphagia.
2. Inability to determine positive predictive value and negative predictive value of bedside
swallowing test due to non-availability of gold standards for detecting dysphagia.
80
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APPENDIX 1: STUDY QUESTIONNAIRE (To be completed by the investigator)
SECTION A:
Please tick the corresponding number provided where applicable
(1) Serial Number: ________________
(2) Hospital Number: __________________________
(3) Name: Surname Other Names:
(4) Age at last Birthday (in Years):_________________
(5) Gender: (1) Male (2) Female
(6) Ethnicity: (1) Hausa (2) Igbo (3) Yoruba
(4) Others Specify____________________________________
(7) Handedness (1) Right (2) Left
(8) Highest Level of Education: (1) Primary (2) Secondary (3Tertiary (4) Postgraduate.
(9) Level of Monthly Income (N):
(1) ≤ 20,000 (2) 20,001- 50,000 (3) 50,001- 100,000 (4) 100,001-200,000
(5) 200,001-500,000 (6)>500,000
(10) Hypertension (1) Yes (2) No Treatment ____________________
If yes, please specify the duration ________________________
(11) Diabetes Mellitus (1) Yes (2) No) Treatment ________________________
If yes, please specify the duration _______________________
(12) Alcohol: (1) Yes (2) No If
If yes, please specify number of beer bottles per week _______________
(13) Smoking: (1) Yes (2) No
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If yes, please specify number of sticks per day ____________________
(14) Date of Presentation: Day Month Year
(15) Date of Discharge: Day Month Year
(16) Date of Demise (where applicable): Day Month Year
SECTION B: PHYSICAL FINDINGS
(18) Glasgow Coma Scale Score: (1) 14 – 15 (2) 9 - 13 (3) 3 – 8
(19) Dysphasia: (1) Present (2) Absent
If present, please specify type ____________________________
(20) Dysarthria: (1) Present (2) Absent
(21) Cranial nerves: (1) Normal (2) Abnormal
If abnormal, please specify ________________________________
(22) Motor weakness: (1) Hemiparesis
(2) Quadriparesis
(3) Monoparesis
(4) Absent
(23) Coordination: (1) Normal (2) Abnormal
(24) Movement Disorder: (1) Present (2) Absent
If present, please specify ______________________________
(25) Pulse: (1) Normal (2) Abnormal
If abnormal, please specify _____________________________
(26) Admitting Blood Pressure: (1) Systolic BP _________________
(2) Diastolic BP __________________
(27) Apex beat: (1) Displaced (2) Not displaced
(28) Heart Murmurs: (1) Present (2) Absent If present, please specify
_________________________________
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(29) Respiratory rate (1) Normal (2) Abnormal
If abnormal please specify --------------------------------------------------
(30) Chest crackles (1) Present (2) Absent
(31)Bronchial breath sound (1) Present (2) Absent
(32) Highest Temperature in the last 24hrs ___________________
(33) Corneal arcus: (1) Present (2) Absent
SECTION C: STROKE DETAILS
(34) Date of Stroke: Day Month Year
(35) Form of Stroke: (1) Ischaemic (2) Hemorrhagic
(36) Stroke Subtype (1) Thrombotic (2) Cardio embolic (3) Artery–to –Artery embolism
(4)Lacunar (5) Intracerebral Haemorrhage (6) Subarachnoid Haemorrhage
(37) Stroke Location (with imaging findings): [May Tick more than one]
(1)One Lobe (2) Multi – Lobar (3) Basal Ganglia (3) Thalamus (4) Watershed
(5)Brainstem (6) Cerebellum (7) TACS (8) PACS (9) POCS
* TACS- Total anterior circulation syndrome
* PACS- Partial anterior circulation syndrome
* POCS- Posterior circulation syndrome
(38) Size of the lesion (From neuroimaging)_____________________________
SECTION D: BEDSIDE SWALLOWING TESTS
(39) Gag Reflex (1) Present (2) Absent
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(40) Water Swallowing Test (WST): (a) 3mls WST (1) Present
(2) Absent
(b) 10mls WST (1) Present
(2) Absent
(c) 30mls WST (1) Present
(2) Absent
(d) 50mls WST (1) Present
(2) Absent
(41) Peripheral oxygen desaturation (1) Present (2) Absent
SECTION E: INVESTIGATIONS
(42) ECG:
(43) Random Plasma Glucose (mg/dl):
(44) Electrolytes (mmol/L): (1) Na+
(2) K+
(3) Cl-
(4) HCO3
(5) Urea (mg/dl)
(45) Full Blood Count (1) White Cell Count ---------------------------------------------------
(2) Platelet Count ----------------------------------------------------
(3) Neutrophil count --------------------------------------------------
(4) Lymphocyte count --------------------------------------------------
(5) Monocyte count ---------------------------------------------------
(46) Chest X- Ray findings (where applicable):
(47) Brain Computerized Tomogram findings: (please refer to No. 37 where applicable)
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(48) Presence of other complications (1) Yes (2) No
If yes, please specify ______________________________________
APPENDIX 2: National Institute of Health Stroke Scale
1a Level of consciousness
0=Alert
1=Not alert, arousable
2=Not alert, obtunded
3=Unresponsive
1b Questions
0=Answers both correctly
1=Answers one correctly
2=Answers neither correctly
1c Commands
0=Performs both tasks correctly
1=Performs one task correctly
2=Performs neither task
2 Gaze
0=Normal
1=Partial gaze palsy
2=Total gaze palsy
3 Visual fields
0=No visual loss
1=Partial hemianopsia
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2=Complete hemianopsia
3=Bilateral hemianopsia
4 Facial palsy
0=Normal
1=Minor paralysis
2=Partial paralysis
3=Complete paralysis
5a Left motor arm
0=No drift
1=Drift before 10 s
2=Falls before 10 s
3=No effort against gravity
4=No movement
5b Right motor arm
0=No drift
1=Drift before 10 s
2=Falls before 10 s
3=No effort against gravity
4=No movement
6a Left motor leg
0=No drift
1=Drift before 5 s
2=Falls before 5 s
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3=No effort against gravity
4=No movement
6b Right motor leg
0=No drift
1=Drift before 5 s
2=Falls before 5 s
3=No effort against gravity
4=No movement
7 Ataxia
0=Absent
1=One limb
2=Two limbs
8 Sensory
0=Normal
1=Mild loss
2=Severe loss
9 Language
0=Normal
1=Mild aphasia
2=Severe aphasia
3=Mute or global aphasia
10 Dysarthria
0=Normal
1=Mild
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2=Severe
11 Extinction/inattention
0=Normal
1=Mild
2=Severe
Patient’s total score: _____________________
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APPENDIX 3: Modified Rankin scale
0=no symptoms
1=no significant disability, despite symptoms
Able to perform all usual duties and activities
2=slight disability
Unable to perform all previous activities but able to look after own affairs without assistance
3=moderate disability
Requires some help, but able to walk without assistance
4=moderately severe disability
Unable to walk without assistance and unable to attend to own bodily needs without assistance
5=severe disability
Bedridden, incontinent, and requires constant nursing care and attention
6=dead
Patient’s score: ________________________
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APPENDIX 4: Barthel index
Bowels
0=Incontinent (or needs to be given enema)
5=Occasional accident (once/week)
10=Continent
Bladder
0=Incontinent, or catheterized and unable to manage
5=Occasional accident (max once per 24 h)
10=Continent (for more than 7 days)
Grooming
0=Needs help with personal care
5=Independent face/hair/teeth/shaving (implements provided)
Toilet use
0=Dependent
5=Needs some help, but can do something alone
10=Independent (on and off, dressing, wiping)
Feeding
0=Unable
5=Needs help cutting, spreading butter, etc.
10=Independent (food provided in reach)
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Transfer
0=Unable, no sitting balance
5=Major help (one or two people, physical), can
10=Minor help (verbal or physical)
15=Independent
Mobility
0=Immobile
5=Wheelchair independent, including corners, etc.
10=Walks with help of one person (verbal or physical)
15=Independent (but may use any aid—e.g., stick)
Dressing
0=Dependent
5=Needs help, but can do about half unaided
10=Independent (including buttons, zips, laces, etc.)
Stairs
0=Unable
5=Needs help (verbal, physical, carrying aid)
10=Independent up and down
Bathing
0=Dependent
5=Independent (or in shower)
Total (0–100)
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Patient’s total score: __________________________
INFORMED CONSENT
My name is Dr Olabode Olajide. I am a staff of the Department of Medicine, University College
Hospital (UCH), Ibadan. I am carrying out a study on patients with stroke at the UCH to find out
if they have difficulty in swallowing. This will be useful in preventing aspiration pneumonitis in
patients with stroke. Aspiration pneumonitis can cause prolong hospital stay or death in stroke
patient.
During this exercise I will need to ask you some questions and carry out physical examination.
This examination will include checking for swallowing difficulty. This will involve touching
back of your throat with a wooden spatula, giving you 10mls of water to drink and attaching
pulse oximeter to your index finger. These procedures will not cause you any harm. Your blood
sample will be taken and sent for random blood glucose and blood electrolytes. The process of
taking the specimen will not cause any harm but a slight pain during the introduction of the
needle. You may be required to do chest x-ray during the course of this study. All the
information obtained will be treated with absolute confidentiality. Appropriate therapy will be
instituted as necessary.
You are free to take part in this study. If you decide not to participate in this study, you will not
be treated differently from any other patients attending this hospital. You have a right to
withdraw from this study anytime you choose. (This will be explained in the vernacular to those
who do not understand English).
If you accept to participate, please indicate below.
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Name……………….........................................................
Signature and Date……………………………………………………………….