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……………………………………………………………….