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CLINICAL EVALUATION OF
LARYNGOPHARYNGEAL REFLUX
AND ITS RESPONSE TO
PROTON PUMP INHIBITORS
In punishment for his wicked ways, the fate of King Sisyphus was to push
a boulder up a hill, almost reaching the peak until the weight of the boulder was such
that it rolled back down the hill only for Sisyphus to restart his eternal and impossible
task over and over again.
It seems that Laryngopharyngeal reflux (LPR) also takes similar course with
otorhinolaryngologists putting diligent efforts to treat the disease but it becomes futile
as soon as the gastric reflux comes up to irritate the laryngeal mucosa starting the
eternal cycle of Laryngopharyngeal reflux.
Introduction
• Laryngopharyngeal reflux disease is a reasonably common
condition, exhibiting a myriad of symptoms and findings referable to the
laryngopharynx and head and neck structures produced by the reflux of
acidic gastric contents.
• The prevalence of the disease ranges from 5 – 30% in western population
whereas in our Indian population it is estimated to be 11% with no sex
predeliction.2
• Laryngopharyngeal reflux is defined as retrograde flow of the stomach
contents to the larynx and pharynx whereby the gastric contents come in
contact with the upper aerodigestive tract. 3,4
• It is synonymously known as reflux laryngitis, silent reflux, extra-
oesophageal reflux, supraoesophageal reflux or silent reflux.
• It represents the extraoesophageal variant of gastroesophageal
disease which affects the larynx and pharynx. Unlike classic
gastric reflux, laryngopharyngeal reflux isn't usually associated
with esophagitis, heartburn, or complaints of regurgitation. It can
present with infinite number of symptoms including :
 hoarseness of voice
 foreign body sensation in throat or globus sensation
 postnasal drip
 sore throat
 difficulty in swallowing
 excessive cough etc.
A number of these symptoms are non-pathognomonic and vague.
At the same time these symptoms simulate the symptoms of grave
diseases of larynx and oesophagus like neoplasm of larynx,
subglottic stenosis emphasizing the importance of early diagnosis
and management of these patients.
Pathophysiology of Laryngopharyngeal reflux
• The lining of the larynx and the hypopharynx is not as protective to gastric acids as the
oesophageal epithelium making it vulnerable to inflammation and tissue injury.
• Not only the gastric acid but other components that are responsible for catalysing
this mucosal inflammation and injury are pepsin, trypsin, bile acids, pancreatic proteolytic
enzymes and bacteria. Some animal studies revealed that at acidic pH levels, it is the pepsin and
conjugated bile acids which cause eminent damage and inflammation to the resistless laryngeal
mucosa and upper digestive tract.5,6
• One more notable cause for laryngopharyngeal reflux is the pressure gradient between
positive intra-abdominal pressure and the negative intrathoracic or intrahypopharyngeal
pressure.
• Some studies also supported the reflexogenic mechanism as a cause of LPR. They stated that
the oesophageal afferents signalling abnormal reflexes in the extraoesophageal structures which
provokes the LPR.7
Disease burden
• The incidence of patients with GERD seeking help of an
Otolaryngologist is estimated to be 4% to 10%.8
• This often leads to high economic and social burdens on patients due
to delay in diagnosis, numerous tertiary care referrals, and lack of
effective medications.
• The economic burden of patients with GERD is estimated to be
$9.3 billion to $12.1 billion, but the cost of treating patients with
extraoesophageal refluxes is 5 times higher, at approximately $50 billion.
9
• The single greatest contributor to the cost of these extraoesophageal
reflux management is the use of proton pump inhibitors (PPIs).
• The literature is littered with inconclusive and incomplete evidences of efficiency of Proton
Pump Inhibitors on laryngopharyngeal reflux which has evoked the need for further research studies
on this topic.
• Moreover, there is no standardised tool for diagnosing laryngopharyngeal reflux. The disease is
currently diagnosed promiscuously on the basis of following three things :
1. Response of symptoms to the empirical proton pump inhibitors treatment.10
2. Endoscopic observation of mucosal inflammation and injury.
3. Demonstration of reflux events by impedance and pH-monitoring studies and barium
swallow esophagogram which are primarily the gold standard invasive investigation for
GERD.
Role of RSI and RFS in diagnosis making
• To provide uniformity in diagnosing the laryngopharyngeal reflux and preventing the
patient to undergo invasive investigations which have low sensitivity and specificity
for laryngopharyngeal reflux, Belafsky et al. came up with two scoring systems :
- Reflux Symptom Index ( RSI ) &
- Reflux Finding Score ( RFS )
for diagnosinglaryngopharyngeal reflux disease.11
• Evidence for establishing the validity of RSI & RFS is scarce requiring further studies to
help providing a diagnostic toolfor laryngopharyngeal reflux.
Reflux symptom index (RSI) is a 9 item self administered outcome instrument.
-It accurately documents symptoms of patients with LPR.
-This index appears to be valid and is highly reproducible. An RSI of more than 13 is considered to indicate LPR.
-It ranges from 0 to 45 (worst possible score).
Reflux finding score (RFS) is an 8 item clinical severity rating scale based on laryngoscopic findings.
-The scale includes most common laryngeal findings related to LPR
- Any individual with RFS greater than 7 has more than 95% probability of having LPR
-RFS accurately document treatment efficacy in patients with LPR.
-It ranges from 0 to 26 (worst score).
Currently in the otolaryngology practice there is
an evolving concern for presently available
diagnosis and management protocol of LPR
which needs to be addressed and worked upon.
Aims & Objectives
To evaluate the patients of laryngopharyngeal reflux and their response to Proton Pump Inhibitors
PRIMARY OBJECTIVE
1. To know the effect of Proton Pump Inhibitors (PPIs) on laryngeal Reflux Symptom Index
(RSI) and Reflux Finding Score (RFS).
SECONDARY OBJECTIVE
1. To know the improvement in signs and symptoms clinically after treatment with Proton Pump
Inhibitors (PPIs).
2. To find the optimal dose and duration of proton pump inhibitorsin treatment of
laryngopharyngeal reflux.
Diagnostic algorithm of Laryngopharyngeal Reflux
• Though there is no perfect diagnostic tool or criteria for laryngopharyngeal reflux
currently, but the management protocol followed involves evaluation of symptoms of
laryngopharyngeal reflux.
• Of utmost importance is to identify the warning symptoms of the patient.
• If there are no warning symptoms patient may be considered for empirical therapy
but in cases of omnius symptoms suggesting pathology other than laryngopharyngeal
reflux patient should be advised for nasopharyngolaryngeal and/or
oesophagogastroduodenoscopic examination.
Tools for
diagnosing
laryngopharyngea
l reflux
1. Reflux Symptom Index (RSI)
 The reflux symptom index (RSI) is a simple
nine-item questionnaire where patients rate the
severity of their LPR symptoms on a Likert scale.
 The symptoms included in the RSI are
hoarseness of voice, throat clearing, post
nasal drip, difficulty in swallowing, annoying
cough, breathing difficulty, cough after
lying down and chest pain.
 The values on scale ranges from 0 to 5 for each
of the nine symptoms, 0 representing no
problem and 5 representing extreme problems.
 The maximum score is 45, and a score above 13
is considered as abnormal acid reflux.11
Reflux Symptom Index (RSI) for Laryngopharyngeal Reflux
Within past 2 months, how did the following problems affect you? Rank them from 0 (no problem) to 5 (severe
problem)
1.Hoarseness or problem with your voice
2.Clearing your throat
3.Excess mucous production in the throat or postnasal drip.
4.Difficulty swallowing food, liquids or pills
5.Coughing after you have eaten or after lying down
6.Breathing difficulty/choking episodes
7.troublesome/annoying cough
8.Sensation of something sticking in your throat or lump in your throat
9.Heartburn, chest pain, indigestion or stomach acid coming up.
2. Laryngoscopic Examination
• Laryngeal endoscopy is performed using flexible transnasal or rigid transoral
laryngoscopes. One prospective study reported that signs of laryngeal irritation
are more often detected with flexible than with rigid laryngoscopes.51
• Laryngoscopic diagnosis of LPR is highly subjective and depends largely on
the expertise and knowledge of the clinician.
• Accurate laryngoscopic assessment of LPR is recondite, and it's not
recommended to form a diagnosis of LPR solely resting on laryngoscopic
results as the laryngeal irritation signs could also be the result of non- reflux
aetiologies, such as allergy, smoking, or voice abuse.
• It is therefore always better to keep in mind the differential diagnoses of LPR.
Reflux Finding Score
• The RFS is an eight-item measure harnessed by clinicians to rate the severity of signs of
inflammation revealed in laryngoscopic examinations as suggested by Belafsky et. al.11
• The signs include subglottic oedema (pseudosulcus), ventricular obliteration, hyperemia,
vocal fold oedema, diffuse laryngeal oedema, posterior commissure hypertrophy, granuloma
and thick endolaryngeal mucus ;values ranging from 0 (normal) to 26 (worst possible score).
• It is a good and convenient method to evaluate treatment responses in LPR patients. The
RFS and RSI both help to fortify the accuracy of LPR diagnoses and evaluate the efficacy of
the treatment provided for the same. Not only less invasive and radiation free tool, it is also a
cost effective one.
• LPR is diagnosed with more conviction in cases where the RSI exceeds 13 along with
RFS exceeds 7.54
Reflux Finding
Score
Laryngoscopic examination showing diffuse erythema Laryngoscopic examination showing hyperemia
Laryngoscopic examination showing Posterior
commissure hypertrophy Laryngoscopic examination showing Thick
endolaryngeal mucus
3. 24-hour dual-sensor pH probe
• The 24-hour dual-sensor pH probe (simultaneous oesophageal and pharyngeal) is the gold
standard investigation for the diagnosis of GERD, with sensitivity of 93.3% and specificity of
90.4%, when employing a cut-off value of 4.5% of total time with pH < 4 during a 24-hour
period.
• Ambulatory pH probe-monitoring is commonly applied to check the efficacy of drug
treatment in cases of LPR.12
• However, it's considered an arbitrary test for confirming LPR because of the
difficulties involved in interpreting pH monitoring data and void of consensus on normal pH
limits, number of events, and probe placement.
• pH probe-monitoring is not apt enough to detect gaseous or nonacid refluxate, which are
potentially harmful to the laryngopharynx. As a result, intraluminal impedance testing is usually
regarded as a superior tool.14
4. Multichannel
Intraluminal Impedance
and pH (MII-pH) Testing
and Hypopharyngeal-
Oesophageal Impedance
with Dual pH Testing
(HEMII-PH)
• Multichannel intraluminal impedance and pH
(MII-pH) catheters allow for acid and non-
acid reflux detection up to the proximal
oesophagus (15 cm above LES).
• There is evidence that MII-pH technology
can be used to improve diagnosis in patients
with suspected LPR.
5.Upper
Gastrointestinal
Endoscopy
• UGE, also called as esophagogastroduodenoscopy
(EGD), can detect signs related to GERD, like
mucosal injury, oesophagitis, Barrett oesophagus,
other complications and malignancies.
• UGE has proven less useful in detecting LPR than
GERD.
• Specialists, like otolaryngologists,
gastroenterologists, and pulmonologists should be
consulted for patients presenting with signs of
complications or malignancies.81
6. Salivary Pepsin
The presence of pepsin in the pharynx is thought by many to be a catalyst for LPR
symptoms. Rapid detection assays for pepsin in saliva are now available.
There is evidence that a positive test for pepsin in the saliva is 78% sensitive and 65%
specific for the diagnosis of oesophagealreflux- related symptoms, and the specificity
increases further when higher pepsin levels are found.
While salivary pepsin measurement is not recommended as a stand-alone diagnostic test
for LPR at this time, it may have value as an adjunct test in certain patient populations.
7. Other Tests
 Barium swallow oesophagograms.
Histomolecular findings including salivary epidermal protein, immunologic markers,
laryngeal mucosa genetic and histologic changes.
Treatment options for
Laryngopharyngeal Reflux
Medical management of laryngopharyngeal reflux should be tailored individually to each patient based on
the nature, frequency, and intensity of symptoms.
These interventions range from pharmacotherapies, such as proton-pump inhibitors and neuromodulators, to
surgical approaches like endoscopic fundoplication. Besides that lifestyle modifications prove to be an
added prophylactic for the adamant disease. Each of the treatment options are described as follows:
A. MEDICAL THERAPY
1. Proton Pump Inhibitors (PPI)
• Proton-pump inhibitors, or PPIs, currently are the first-line treatment for GERD manifested by more than
rare (less than weekly) symptoms.
• MOA: PPIs suppress acid by inhibiting the H+/K+-ATPase transporter involved in the final step of gastric
acid secretion.
• Omeprazole was the first PPI developed followed by lansoprazole. For symptomatic GERD, an 8-week trial
of once-daily dosing generally is recommended, although for severe refractory reflux, patients respond well
to twice-daily dosing for a minimum of 8 weeks.
• For maximum efficacy in terms of inhibiting acid secretion, most PPIs should be taken 0.5–1
hour prior to meals.
• However, Dexlansoprazole has a dual release mechanism, containing two types of delayed-
release granules. The first type of granules readily releases the medication with peak
concentration achieved within 1–2 hours of administration. The second type slowly releases the
drug, achieving a second peak about 4–5 hours after administration. As a result, dexlansoprazole
offers the advantage of convenience to patients, as this PPI can be administered at any
time, independent of meals.
• Similarly, patients can experience a more immediate benefit from taking the omeprazole with
sodium bicarbonate, an immediate-release PPI. This combination often has been used for
patients with significant nocturnal symptoms, as omeprazole- sodium bicarbonate controls
nocturnal gastric pH in the first few hours of sleep or laying supine when compared to other
PPIs taken at bedtime.
• In maintenance therapy, their long-term safety is an important issue to discuss with
all patients.
• Potential adverse effects associated with PPI use include nutritional deficiencies, enteric
infections such as Clostridium difficile colitis, kidney disease, community-acquired
pneumonia, osteoporosis and bone fracture, and even dementia, as well as cardiovascular
events in patients using concomitant clopidogrel therapy.
• PPIs confer effective gastric acid suppression; however, gastric acid is often a necessary step
in absorption of vitamins, such as vitamin B12 (cobalamin). Initially, cobalamin absorption
relies on gastric acid, and evidence suggests that B12 deficiency is more likely to develop in
institutionalized elderly patients on long-term PPI therapy.
• PPIs also have other drawbacks, including risks of adverse cardiovascular events,
osteoporosis and bone fractures, and hospital-acquired pneumonia. PPIs interact with
clopidogrel via the CYP2C19 pathway. Moreover, in vitro studies established that PPIs limit
clopidogrel’s efficacy in disrupting platelet aggregation.97,98
Adverse effects of PPI:
• Reduction of gastric acid has also been associated with decreased
mobilization of ionized calcium, potentially increasing risk of osteoporosis
and eventual bone fracture. Some studies have documented increased risk of
community-acquired pneumonia in patients taking PPIs only short term.
• Ultimately, according to existing research, benefits from PPI use outweigh
risks. As a result, clinicians should be not be averse to prescribing PPIs to
avoid risks that are thus far only weakly and/or inconsistently associated
with their long- and short-term use.
Proton Pump Inhibitors and their dosage and adverse reactions
2. Prokinetics
3.Macrolide antibiotics
4.Histamine antagonists
5.GABA agonists
6.Alginates
7.Neuromodulators
Alternative treatment
Impact of lifestyle modification on laryngopharyngeal
reflux
1.DIET
• Fatty and acidic diet worsens reflux symptoms. Specifically, duodenal fat is thought to cause
gastric distension, lower oesophageal sphincter (LES) relaxation, and increased visceral
sensitivity compared to glucose-rich meals, explaining some of the classic dyspepsia
symptoms.
• Changes in symptoms of the fasting group may be attributed to alterations in gastric acid and
pepsin secretions, which increase during the fasting state.
• Eating smaller, more frequent meals and avoid long time periods with an empty
stomach. Avoidance of chocolate, caffeine, citrus, and spicy and acidic foods,
carbonated beverages, coffee, chocolate, and spicy foods may be associated with
improvement in laryngopharyngeal reflux by pH probe.
• The effect of meal-timing on reflux has also been investigated. Specifically, avoiding late
meals has been shown to significantly decrease gastric and oesophageal acidity.
2. Exercise
 Though there are no studies directly correlating exercise and LPR,
several examine its effects on gastroesophageal reflux. Nilsson et al.
demonstrated a decreased association of reflux in those who exercised in a
cross-sectional observational study.
 Furthermore, even in subjects with a diagnosis of GERD, the symptoms of
reflux were found to be less severe in the subset who exercise.
3. Smoking and Alcohol
 Although traditional antireflux diets include the elimination of alcohol
and tobacco, their effect on reflux is not clear
Materials and methods
• This prospective observational study was conducted on 128 patients attending the
Otolaryngology OPD of VSSIMSAR, Burla from July 2018 till October 2020 who had
persistent laryngeal symptoms for more than 2 months.
• A total of 170 subjects were screened and assessed to meet the criteria set
for including subjects in the study. 19 patients did not meet inclusion criteria while 8
were unwilling for participating in the study. 10 patients lost to follow up while 5
patients were found to be non-compliant to the treatment and were thus excluded from the
study.
Data collected using standardized Reflux Scoring Index (RSI) and
Reflux Finding score (RFS) after taking detailed history and performing
complete clinical examination. An English/ Hindi/ Odiya translated RSI
table was given to the patient to read and respond to the questions;
those who could not read the research assistant read to them the
questions and asked to provide answers to fill the Reflux Scoring
Index (RSI) table by circling the number corresponding to patients score
on specific questions answering the reflux scoring index and the RSI
≥13 was regarded as one of the inclusion criteria for the study. Other
prerequisite inclusion and exclusion criteria used are as follows :
Inclusion criteria
• Female or male ≥ 18 years of age.
• Patient with symptoms suggestive of LPRD with a reflux
symptom index (RSI) ≥ 13 in any of symptom score.
• Patient with signs suggestive of LPRD with reflux finding
score (RFS) ≥ 7 as per laryngeal endoscopic examination.
• Written informed consent.
1.Continuous treatment with any acid‐suppressive drug for 7 days or more within the last 4
weeks before inclusion in the study
2.Contraindications/ hypersensitive to Proton Pump Inhibitor treatment.
3.Patient with rhinosinusitis, allergy, benign and malignant vocal cord lesions.
4.Patients with other coexisting laryngeal pathology.
5.Those who are on any regular drugs.
6.Gastroesophageal reflux disease or other oesophageal dysmotility disorder.
7.Any ‘alarm symptoms’ like significant weight loss, haematemesis, melaena, fever, jaundice or
the other sign indicating serious or malignant disease (suspected or confirmed malignancy) or
other significant cardiovascular, pulmonary (e.g. severe emphysema), renal, pancreatic or
disease likely to interfere with study procedure.
8.Pregnancy and lactation.
Exclusion criteria
• All Patients with RSI ≥ 13 then underwent laryngoscopic examination so as to determine their Reflux
Finding Score (RFS).
• The patients were advised to stay empty stomach for atleast 1 hour before the laryngeal endoscopy to
prevent discomfort and refluxes during the procedure.
• 10% xylocaine local anaesthetic solution was sprayed in the posterior pharyngeal wall of the patients
and were asked to swallow the solution. 10 minutes later, when their hypopharynx and larynx showed
the effect of local anaesthetic solution, laryngeal endoscopy was performed holding the tongue of the
patient with gauze piece in left hand and endoscope in right.
• A 700 Karl Storz rigid laryngoscope was then introduced into the oral cavity of the patient to reach the
hypopharynx and larynx.
• All the structure were examined with great detail starting from oropharynx including base of
tongue, epiglottis, vallecula, pyriform sinus, post cricoid area, bilateral arytenoids and aryepiglottic
folds, bilateral ventricular folds, bilateral vocal folds along with anterior and posterior commissures
and the subglottic area.
• For those patients who could not be evaluated with rigid laryngoscope, a flexible
nasopharyngolaryngoscope was done.
• A total Reflux Finding Score (RFS) of 7 was regarded as diagnostic of laryngopharyngeal reflux. The
result obtained was documented in the Reflux Finding Score (RFS) Performa sheet.
• The patients who were diagnosed of laryngopharyngeal reflux on the basis of their
Reflux Symptom Index (RSI) & Reflux Finding Score (RFS) were subjected to the
treatment of Pantoprazole 40 mg twice daily for a duration of six months taken
on empty stomach.
• The patients were called back for follow up at 2nd, 4th and 6th months of initiation of
Proton Pump Inhibitor treatment.
• On each follow up visit patients symptoms were evaluated for their Reflux
Symptom Index (RSI) & Reflux Finding Score (RFS). Laryngoscopy also
evaluated vocal fold lesions and other complications of the reflux disease.
• Chest X-ray and ECG were done for the patients with complain of breathing
difficulty to exclude chest problem and heart diseases.
• Patients who didn’t meet diagnostic points were sent for upper gastrointestinal
endoscopy and were further treated according to their illness.
• The data were tested for homogeneity variances prior to further statistical analysis.
Categorical variables were described by number and percent (n , %),
where continuous variables described by mean and standard deviation (Mean ± SD).
• All analyses were performed using statistical package of social science SPSS 20.0
software. Wilcoxon signed rank test was used for comparison of the paired data of
two sets.
• A p-value of < 0.01 was considered to be statistically significant.
• The results are presented in frequency tables, bar diagrams, pie charts and other
illustrative methods.
OBSERVATIONS AND RESULTS
 The observation and results are evaluated and plotted with a total of 128 patients (n=128). The demographic
characteristics taken in our study were gender, age and educational qualification.
 Among the 128 patients, 55 were males (42.97%) and 73 were females (57.03%) : data exhibiting female predominance in
laryngopharyngeal reflux patients.
43%
57%
Age&
gender
distribution
• In our study, the age distribution data showed that the
maximum number of patients were of age group 28-37
years i.e. 38( 29.69%) patients followed by age group of
38 – 47 years (24.22%). And least number of cases were
seen in age group ≥ 58 years, i.e. 14 (10.94%) patients.
• The mean age was 39 years with minimum age of 19 and
maximum of 77 years in the study population.
• Thus the age and gender distribution of the study
proclaimed Laryngopharyngeal reflux disease to be
prevalent in middle age group population with female
predominance.
Age distribution in the study population
Etiological factors in laryngopharyngeal reflux patients
 Out of 128, 77 patients were habituated to tea/ coffee/caffeinated beverages accounting to 60.16% of the
total study population.
 Other common etiological factors noted were fried/fatty food and less sleep, observed in 63 and 57
patients, respectively.
 This shows that the most common etiology for LPR is tea/ coffee/caffeinated beverages.
Educational qualification of LPR patients
 The study revealed the fact that Laryngopharyngeal reflux was more prevalent in patients of higher
educational status.
 Out of 128 patients, 73 (57.03%) patients having LPR owned academic degree or higher education.
The prevalence of LPR is less among people who could not complete their high school education.
Prevalence of
various
symptoms in
LPR
suspected
patients
 The two most troublesome symptom as mentioned by the patients were foreign body sensation
throat/ globus sensation followed by hoarseness of voice, found in 121(94.53%) and 117
(91.41%) patients, respectively.
 Other complains include :
throat clearing in 11(88.28%),
cough after eating/lying down in 102 (79.69%),
annoying cough in 100 (78.13%),
excess mucus or post nasal discharge in 92 (71.88%),
heartburn in 72 (56.25%) patients.
 Least commonly mentioned symptoms were breathing difficulty and difficulty in swallowing,
observed by 20 (15.63%) and 22 (17.19%) patients of laryngopharyngeal reflux, respectively .
Prevalence of various symptoms in LPR suspected patients
Endoscopic findings among patients with laryngopharyngeal
reflux before and after Proton Pump Inhibitor
treatment
The laryngoscopic examination showed that the most common sign of laryngeal inflammation
observed in our study population was erythema which was found in 121 (94.53%) patients
followed by thick laryngeal mucosa in 116 (90.63%) patients.
Other signs observed were:
posterior commissure hypertrophy in 113 (88.28%),
vocal fold oedema in 95(74.22%),
diffuse laryngeal oedema in 90 (70.31%),
ventricular oedema in 77 (60.16%) &
subglottic oedema in 40 (31.25%).
The least commonly seen sign on laryngeal endoscopy was granuloma, found in 18 (14.06%)
patients.
Endoscopic findings among
patients with LPR before and
after Proton
Pump Inhibitor treatment
The overall effect of PPI on all the symptoms of LPR included in
RSI is statistically significant except on the swallowing difficulty
where improvement was there but not statistically significant at
p<0.01.
The study elucidated that PPI are effective in relieving the
symptoms of LPR patients .
Improvement of laryngeal symptoms
after the PPI treatment
Improvement of
laryngeal
symptoms after the
PPI treatment
The final data interpretation was for the comparison of RSI and RFS before and after the PPI treatment and the corelation
between RSI & RFS :
Using Wilcoxon signed rank test, z -9.817; p value
<0.0001
The RSI ≥13 was our inclusion criteria, therefore all of
the 128 patients showed RSI ≥ 13. But after the PPI treatment,
RSI improved significantly in all 128 patients. The average
RSI before treatment was 20 which dropped down significantly
to average of 4 after PPI treatment and the result was
significant at p<0.01
Comparison between RSI before and after PPI treatment
 The study showed that average RFS before
PPI treatment was 12 and after the PPI
treatment it improved significantly to average
of 3.594 ~4.
 The result was significant at p<0.01. Before
initiation of treatment, all of 128 patients had
RFS ≥ 7 and this no. decreased substantially
after the treatment to RFS < 7 in 109 patients.
Comparison between RFS before and after PPI treatment
Evaluating Pearson correlation coefficient,
the value of R = 0.3717 ; R2 = 0.1382
showing positive correlation between the RSI
& RFS.
The result signifies that RSI & RFS are related to
each other and any change in the RSI will affect the
value of RFI and vice versa.
Also p=0.000016 so the result is significant
at p<0.01.
Correlation between RSI and RFS
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Clinical evaluation of Laryngopharyngeal reflux and its response to Proton Pump Inhibitors

  • 1. CLINICAL EVALUATION OF LARYNGOPHARYNGEAL REFLUX AND ITS RESPONSE TO PROTON PUMP INHIBITORS
  • 2. In punishment for his wicked ways, the fate of King Sisyphus was to push a boulder up a hill, almost reaching the peak until the weight of the boulder was such that it rolled back down the hill only for Sisyphus to restart his eternal and impossible task over and over again. It seems that Laryngopharyngeal reflux (LPR) also takes similar course with otorhinolaryngologists putting diligent efforts to treat the disease but it becomes futile as soon as the gastric reflux comes up to irritate the laryngeal mucosa starting the eternal cycle of Laryngopharyngeal reflux.
  • 3. Introduction • Laryngopharyngeal reflux disease is a reasonably common condition, exhibiting a myriad of symptoms and findings referable to the laryngopharynx and head and neck structures produced by the reflux of acidic gastric contents. • The prevalence of the disease ranges from 5 – 30% in western population whereas in our Indian population it is estimated to be 11% with no sex predeliction.2 • Laryngopharyngeal reflux is defined as retrograde flow of the stomach contents to the larynx and pharynx whereby the gastric contents come in contact with the upper aerodigestive tract. 3,4 • It is synonymously known as reflux laryngitis, silent reflux, extra- oesophageal reflux, supraoesophageal reflux or silent reflux.
  • 4. • It represents the extraoesophageal variant of gastroesophageal disease which affects the larynx and pharynx. Unlike classic gastric reflux, laryngopharyngeal reflux isn't usually associated with esophagitis, heartburn, or complaints of regurgitation. It can present with infinite number of symptoms including :  hoarseness of voice  foreign body sensation in throat or globus sensation  postnasal drip  sore throat  difficulty in swallowing  excessive cough etc. A number of these symptoms are non-pathognomonic and vague. At the same time these symptoms simulate the symptoms of grave diseases of larynx and oesophagus like neoplasm of larynx, subglottic stenosis emphasizing the importance of early diagnosis and management of these patients.
  • 6. • The lining of the larynx and the hypopharynx is not as protective to gastric acids as the oesophageal epithelium making it vulnerable to inflammation and tissue injury. • Not only the gastric acid but other components that are responsible for catalysing this mucosal inflammation and injury are pepsin, trypsin, bile acids, pancreatic proteolytic enzymes and bacteria. Some animal studies revealed that at acidic pH levels, it is the pepsin and conjugated bile acids which cause eminent damage and inflammation to the resistless laryngeal mucosa and upper digestive tract.5,6 • One more notable cause for laryngopharyngeal reflux is the pressure gradient between positive intra-abdominal pressure and the negative intrathoracic or intrahypopharyngeal pressure. • Some studies also supported the reflexogenic mechanism as a cause of LPR. They stated that the oesophageal afferents signalling abnormal reflexes in the extraoesophageal structures which provokes the LPR.7
  • 7. Disease burden • The incidence of patients with GERD seeking help of an Otolaryngologist is estimated to be 4% to 10%.8 • This often leads to high economic and social burdens on patients due to delay in diagnosis, numerous tertiary care referrals, and lack of effective medications. • The economic burden of patients with GERD is estimated to be $9.3 billion to $12.1 billion, but the cost of treating patients with extraoesophageal refluxes is 5 times higher, at approximately $50 billion. 9 • The single greatest contributor to the cost of these extraoesophageal reflux management is the use of proton pump inhibitors (PPIs).
  • 8. • The literature is littered with inconclusive and incomplete evidences of efficiency of Proton Pump Inhibitors on laryngopharyngeal reflux which has evoked the need for further research studies on this topic. • Moreover, there is no standardised tool for diagnosing laryngopharyngeal reflux. The disease is currently diagnosed promiscuously on the basis of following three things : 1. Response of symptoms to the empirical proton pump inhibitors treatment.10 2. Endoscopic observation of mucosal inflammation and injury. 3. Demonstration of reflux events by impedance and pH-monitoring studies and barium swallow esophagogram which are primarily the gold standard invasive investigation for GERD.
  • 9. Role of RSI and RFS in diagnosis making • To provide uniformity in diagnosing the laryngopharyngeal reflux and preventing the patient to undergo invasive investigations which have low sensitivity and specificity for laryngopharyngeal reflux, Belafsky et al. came up with two scoring systems : - Reflux Symptom Index ( RSI ) & - Reflux Finding Score ( RFS ) for diagnosinglaryngopharyngeal reflux disease.11 • Evidence for establishing the validity of RSI & RFS is scarce requiring further studies to help providing a diagnostic toolfor laryngopharyngeal reflux.
  • 10. Reflux symptom index (RSI) is a 9 item self administered outcome instrument. -It accurately documents symptoms of patients with LPR. -This index appears to be valid and is highly reproducible. An RSI of more than 13 is considered to indicate LPR. -It ranges from 0 to 45 (worst possible score). Reflux finding score (RFS) is an 8 item clinical severity rating scale based on laryngoscopic findings. -The scale includes most common laryngeal findings related to LPR - Any individual with RFS greater than 7 has more than 95% probability of having LPR -RFS accurately document treatment efficacy in patients with LPR. -It ranges from 0 to 26 (worst score).
  • 11. Currently in the otolaryngology practice there is an evolving concern for presently available diagnosis and management protocol of LPR which needs to be addressed and worked upon.
  • 12. Aims & Objectives To evaluate the patients of laryngopharyngeal reflux and their response to Proton Pump Inhibitors PRIMARY OBJECTIVE 1. To know the effect of Proton Pump Inhibitors (PPIs) on laryngeal Reflux Symptom Index (RSI) and Reflux Finding Score (RFS). SECONDARY OBJECTIVE 1. To know the improvement in signs and symptoms clinically after treatment with Proton Pump Inhibitors (PPIs). 2. To find the optimal dose and duration of proton pump inhibitorsin treatment of laryngopharyngeal reflux.
  • 13. Diagnostic algorithm of Laryngopharyngeal Reflux
  • 14. • Though there is no perfect diagnostic tool or criteria for laryngopharyngeal reflux currently, but the management protocol followed involves evaluation of symptoms of laryngopharyngeal reflux. • Of utmost importance is to identify the warning symptoms of the patient. • If there are no warning symptoms patient may be considered for empirical therapy but in cases of omnius symptoms suggesting pathology other than laryngopharyngeal reflux patient should be advised for nasopharyngolaryngeal and/or oesophagogastroduodenoscopic examination.
  • 15. Tools for diagnosing laryngopharyngea l reflux 1. Reflux Symptom Index (RSI)  The reflux symptom index (RSI) is a simple nine-item questionnaire where patients rate the severity of their LPR symptoms on a Likert scale.  The symptoms included in the RSI are hoarseness of voice, throat clearing, post nasal drip, difficulty in swallowing, annoying cough, breathing difficulty, cough after lying down and chest pain.  The values on scale ranges from 0 to 5 for each of the nine symptoms, 0 representing no problem and 5 representing extreme problems.  The maximum score is 45, and a score above 13 is considered as abnormal acid reflux.11
  • 16. Reflux Symptom Index (RSI) for Laryngopharyngeal Reflux Within past 2 months, how did the following problems affect you? Rank them from 0 (no problem) to 5 (severe problem) 1.Hoarseness or problem with your voice 2.Clearing your throat 3.Excess mucous production in the throat or postnasal drip. 4.Difficulty swallowing food, liquids or pills 5.Coughing after you have eaten or after lying down 6.Breathing difficulty/choking episodes 7.troublesome/annoying cough 8.Sensation of something sticking in your throat or lump in your throat 9.Heartburn, chest pain, indigestion or stomach acid coming up.
  • 17. 2. Laryngoscopic Examination • Laryngeal endoscopy is performed using flexible transnasal or rigid transoral laryngoscopes. One prospective study reported that signs of laryngeal irritation are more often detected with flexible than with rigid laryngoscopes.51 • Laryngoscopic diagnosis of LPR is highly subjective and depends largely on the expertise and knowledge of the clinician. • Accurate laryngoscopic assessment of LPR is recondite, and it's not recommended to form a diagnosis of LPR solely resting on laryngoscopic results as the laryngeal irritation signs could also be the result of non- reflux aetiologies, such as allergy, smoking, or voice abuse. • It is therefore always better to keep in mind the differential diagnoses of LPR.
  • 18. Reflux Finding Score • The RFS is an eight-item measure harnessed by clinicians to rate the severity of signs of inflammation revealed in laryngoscopic examinations as suggested by Belafsky et. al.11 • The signs include subglottic oedema (pseudosulcus), ventricular obliteration, hyperemia, vocal fold oedema, diffuse laryngeal oedema, posterior commissure hypertrophy, granuloma and thick endolaryngeal mucus ;values ranging from 0 (normal) to 26 (worst possible score). • It is a good and convenient method to evaluate treatment responses in LPR patients. The RFS and RSI both help to fortify the accuracy of LPR diagnoses and evaluate the efficacy of the treatment provided for the same. Not only less invasive and radiation free tool, it is also a cost effective one. • LPR is diagnosed with more conviction in cases where the RSI exceeds 13 along with RFS exceeds 7.54
  • 20. Laryngoscopic examination showing diffuse erythema Laryngoscopic examination showing hyperemia
  • 21. Laryngoscopic examination showing Posterior commissure hypertrophy Laryngoscopic examination showing Thick endolaryngeal mucus
  • 22. 3. 24-hour dual-sensor pH probe • The 24-hour dual-sensor pH probe (simultaneous oesophageal and pharyngeal) is the gold standard investigation for the diagnosis of GERD, with sensitivity of 93.3% and specificity of 90.4%, when employing a cut-off value of 4.5% of total time with pH < 4 during a 24-hour period. • Ambulatory pH probe-monitoring is commonly applied to check the efficacy of drug treatment in cases of LPR.12 • However, it's considered an arbitrary test for confirming LPR because of the difficulties involved in interpreting pH monitoring data and void of consensus on normal pH limits, number of events, and probe placement. • pH probe-monitoring is not apt enough to detect gaseous or nonacid refluxate, which are potentially harmful to the laryngopharynx. As a result, intraluminal impedance testing is usually regarded as a superior tool.14
  • 23. 4. Multichannel Intraluminal Impedance and pH (MII-pH) Testing and Hypopharyngeal- Oesophageal Impedance with Dual pH Testing (HEMII-PH) • Multichannel intraluminal impedance and pH (MII-pH) catheters allow for acid and non- acid reflux detection up to the proximal oesophagus (15 cm above LES). • There is evidence that MII-pH technology can be used to improve diagnosis in patients with suspected LPR.
  • 24. 5.Upper Gastrointestinal Endoscopy • UGE, also called as esophagogastroduodenoscopy (EGD), can detect signs related to GERD, like mucosal injury, oesophagitis, Barrett oesophagus, other complications and malignancies. • UGE has proven less useful in detecting LPR than GERD. • Specialists, like otolaryngologists, gastroenterologists, and pulmonologists should be consulted for patients presenting with signs of complications or malignancies.81
  • 25. 6. Salivary Pepsin The presence of pepsin in the pharynx is thought by many to be a catalyst for LPR symptoms. Rapid detection assays for pepsin in saliva are now available. There is evidence that a positive test for pepsin in the saliva is 78% sensitive and 65% specific for the diagnosis of oesophagealreflux- related symptoms, and the specificity increases further when higher pepsin levels are found. While salivary pepsin measurement is not recommended as a stand-alone diagnostic test for LPR at this time, it may have value as an adjunct test in certain patient populations. 7. Other Tests  Barium swallow oesophagograms. Histomolecular findings including salivary epidermal protein, immunologic markers, laryngeal mucosa genetic and histologic changes.
  • 26. Treatment options for Laryngopharyngeal Reflux Medical management of laryngopharyngeal reflux should be tailored individually to each patient based on the nature, frequency, and intensity of symptoms. These interventions range from pharmacotherapies, such as proton-pump inhibitors and neuromodulators, to surgical approaches like endoscopic fundoplication. Besides that lifestyle modifications prove to be an added prophylactic for the adamant disease. Each of the treatment options are described as follows: A. MEDICAL THERAPY 1. Proton Pump Inhibitors (PPI) • Proton-pump inhibitors, or PPIs, currently are the first-line treatment for GERD manifested by more than rare (less than weekly) symptoms. • MOA: PPIs suppress acid by inhibiting the H+/K+-ATPase transporter involved in the final step of gastric acid secretion. • Omeprazole was the first PPI developed followed by lansoprazole. For symptomatic GERD, an 8-week trial of once-daily dosing generally is recommended, although for severe refractory reflux, patients respond well to twice-daily dosing for a minimum of 8 weeks.
  • 27. • For maximum efficacy in terms of inhibiting acid secretion, most PPIs should be taken 0.5–1 hour prior to meals. • However, Dexlansoprazole has a dual release mechanism, containing two types of delayed- release granules. The first type of granules readily releases the medication with peak concentration achieved within 1–2 hours of administration. The second type slowly releases the drug, achieving a second peak about 4–5 hours after administration. As a result, dexlansoprazole offers the advantage of convenience to patients, as this PPI can be administered at any time, independent of meals. • Similarly, patients can experience a more immediate benefit from taking the omeprazole with sodium bicarbonate, an immediate-release PPI. This combination often has been used for patients with significant nocturnal symptoms, as omeprazole- sodium bicarbonate controls nocturnal gastric pH in the first few hours of sleep or laying supine when compared to other PPIs taken at bedtime.
  • 28. • In maintenance therapy, their long-term safety is an important issue to discuss with all patients. • Potential adverse effects associated with PPI use include nutritional deficiencies, enteric infections such as Clostridium difficile colitis, kidney disease, community-acquired pneumonia, osteoporosis and bone fracture, and even dementia, as well as cardiovascular events in patients using concomitant clopidogrel therapy. • PPIs confer effective gastric acid suppression; however, gastric acid is often a necessary step in absorption of vitamins, such as vitamin B12 (cobalamin). Initially, cobalamin absorption relies on gastric acid, and evidence suggests that B12 deficiency is more likely to develop in institutionalized elderly patients on long-term PPI therapy. • PPIs also have other drawbacks, including risks of adverse cardiovascular events, osteoporosis and bone fractures, and hospital-acquired pneumonia. PPIs interact with clopidogrel via the CYP2C19 pathway. Moreover, in vitro studies established that PPIs limit clopidogrel’s efficacy in disrupting platelet aggregation.97,98 Adverse effects of PPI:
  • 29. • Reduction of gastric acid has also been associated with decreased mobilization of ionized calcium, potentially increasing risk of osteoporosis and eventual bone fracture. Some studies have documented increased risk of community-acquired pneumonia in patients taking PPIs only short term. • Ultimately, according to existing research, benefits from PPI use outweigh risks. As a result, clinicians should be not be averse to prescribing PPIs to avoid risks that are thus far only weakly and/or inconsistently associated with their long- and short-term use.
  • 30. Proton Pump Inhibitors and their dosage and adverse reactions
  • 31. 2. Prokinetics 3.Macrolide antibiotics 4.Histamine antagonists 5.GABA agonists 6.Alginates 7.Neuromodulators
  • 33. Impact of lifestyle modification on laryngopharyngeal reflux 1.DIET • Fatty and acidic diet worsens reflux symptoms. Specifically, duodenal fat is thought to cause gastric distension, lower oesophageal sphincter (LES) relaxation, and increased visceral sensitivity compared to glucose-rich meals, explaining some of the classic dyspepsia symptoms. • Changes in symptoms of the fasting group may be attributed to alterations in gastric acid and pepsin secretions, which increase during the fasting state. • Eating smaller, more frequent meals and avoid long time periods with an empty stomach. Avoidance of chocolate, caffeine, citrus, and spicy and acidic foods, carbonated beverages, coffee, chocolate, and spicy foods may be associated with improvement in laryngopharyngeal reflux by pH probe. • The effect of meal-timing on reflux has also been investigated. Specifically, avoiding late meals has been shown to significantly decrease gastric and oesophageal acidity.
  • 34. 2. Exercise  Though there are no studies directly correlating exercise and LPR, several examine its effects on gastroesophageal reflux. Nilsson et al. demonstrated a decreased association of reflux in those who exercised in a cross-sectional observational study.  Furthermore, even in subjects with a diagnosis of GERD, the symptoms of reflux were found to be less severe in the subset who exercise. 3. Smoking and Alcohol  Although traditional antireflux diets include the elimination of alcohol and tobacco, their effect on reflux is not clear
  • 35.
  • 36. Materials and methods • This prospective observational study was conducted on 128 patients attending the Otolaryngology OPD of VSSIMSAR, Burla from July 2018 till October 2020 who had persistent laryngeal symptoms for more than 2 months. • A total of 170 subjects were screened and assessed to meet the criteria set for including subjects in the study. 19 patients did not meet inclusion criteria while 8 were unwilling for participating in the study. 10 patients lost to follow up while 5 patients were found to be non-compliant to the treatment and were thus excluded from the study.
  • 37. Data collected using standardized Reflux Scoring Index (RSI) and Reflux Finding score (RFS) after taking detailed history and performing complete clinical examination. An English/ Hindi/ Odiya translated RSI table was given to the patient to read and respond to the questions; those who could not read the research assistant read to them the questions and asked to provide answers to fill the Reflux Scoring Index (RSI) table by circling the number corresponding to patients score on specific questions answering the reflux scoring index and the RSI ≥13 was regarded as one of the inclusion criteria for the study. Other prerequisite inclusion and exclusion criteria used are as follows :
  • 38. Inclusion criteria • Female or male ≥ 18 years of age. • Patient with symptoms suggestive of LPRD with a reflux symptom index (RSI) ≥ 13 in any of symptom score. • Patient with signs suggestive of LPRD with reflux finding score (RFS) ≥ 7 as per laryngeal endoscopic examination. • Written informed consent.
  • 39. 1.Continuous treatment with any acid‐suppressive drug for 7 days or more within the last 4 weeks before inclusion in the study 2.Contraindications/ hypersensitive to Proton Pump Inhibitor treatment. 3.Patient with rhinosinusitis, allergy, benign and malignant vocal cord lesions. 4.Patients with other coexisting laryngeal pathology. 5.Those who are on any regular drugs. 6.Gastroesophageal reflux disease or other oesophageal dysmotility disorder. 7.Any ‘alarm symptoms’ like significant weight loss, haematemesis, melaena, fever, jaundice or the other sign indicating serious or malignant disease (suspected or confirmed malignancy) or other significant cardiovascular, pulmonary (e.g. severe emphysema), renal, pancreatic or disease likely to interfere with study procedure. 8.Pregnancy and lactation. Exclusion criteria
  • 40. • All Patients with RSI ≥ 13 then underwent laryngoscopic examination so as to determine their Reflux Finding Score (RFS). • The patients were advised to stay empty stomach for atleast 1 hour before the laryngeal endoscopy to prevent discomfort and refluxes during the procedure. • 10% xylocaine local anaesthetic solution was sprayed in the posterior pharyngeal wall of the patients and were asked to swallow the solution. 10 minutes later, when their hypopharynx and larynx showed the effect of local anaesthetic solution, laryngeal endoscopy was performed holding the tongue of the patient with gauze piece in left hand and endoscope in right. • A 700 Karl Storz rigid laryngoscope was then introduced into the oral cavity of the patient to reach the hypopharynx and larynx. • All the structure were examined with great detail starting from oropharynx including base of tongue, epiglottis, vallecula, pyriform sinus, post cricoid area, bilateral arytenoids and aryepiglottic folds, bilateral ventricular folds, bilateral vocal folds along with anterior and posterior commissures and the subglottic area. • For those patients who could not be evaluated with rigid laryngoscope, a flexible nasopharyngolaryngoscope was done. • A total Reflux Finding Score (RFS) of 7 was regarded as diagnostic of laryngopharyngeal reflux. The result obtained was documented in the Reflux Finding Score (RFS) Performa sheet.
  • 41. • The patients who were diagnosed of laryngopharyngeal reflux on the basis of their Reflux Symptom Index (RSI) & Reflux Finding Score (RFS) were subjected to the treatment of Pantoprazole 40 mg twice daily for a duration of six months taken on empty stomach. • The patients were called back for follow up at 2nd, 4th and 6th months of initiation of Proton Pump Inhibitor treatment. • On each follow up visit patients symptoms were evaluated for their Reflux Symptom Index (RSI) & Reflux Finding Score (RFS). Laryngoscopy also evaluated vocal fold lesions and other complications of the reflux disease. • Chest X-ray and ECG were done for the patients with complain of breathing difficulty to exclude chest problem and heart diseases. • Patients who didn’t meet diagnostic points were sent for upper gastrointestinal endoscopy and were further treated according to their illness.
  • 42. • The data were tested for homogeneity variances prior to further statistical analysis. Categorical variables were described by number and percent (n , %), where continuous variables described by mean and standard deviation (Mean ± SD). • All analyses were performed using statistical package of social science SPSS 20.0 software. Wilcoxon signed rank test was used for comparison of the paired data of two sets. • A p-value of < 0.01 was considered to be statistically significant. • The results are presented in frequency tables, bar diagrams, pie charts and other illustrative methods.
  • 43. OBSERVATIONS AND RESULTS  The observation and results are evaluated and plotted with a total of 128 patients (n=128). The demographic characteristics taken in our study were gender, age and educational qualification.  Among the 128 patients, 55 were males (42.97%) and 73 were females (57.03%) : data exhibiting female predominance in laryngopharyngeal reflux patients. 43% 57%
  • 44. Age& gender distribution • In our study, the age distribution data showed that the maximum number of patients were of age group 28-37 years i.e. 38( 29.69%) patients followed by age group of 38 – 47 years (24.22%). And least number of cases were seen in age group ≥ 58 years, i.e. 14 (10.94%) patients. • The mean age was 39 years with minimum age of 19 and maximum of 77 years in the study population. • Thus the age and gender distribution of the study proclaimed Laryngopharyngeal reflux disease to be prevalent in middle age group population with female predominance.
  • 45. Age distribution in the study population
  • 46. Etiological factors in laryngopharyngeal reflux patients  Out of 128, 77 patients were habituated to tea/ coffee/caffeinated beverages accounting to 60.16% of the total study population.  Other common etiological factors noted were fried/fatty food and less sleep, observed in 63 and 57 patients, respectively.  This shows that the most common etiology for LPR is tea/ coffee/caffeinated beverages.
  • 47. Educational qualification of LPR patients  The study revealed the fact that Laryngopharyngeal reflux was more prevalent in patients of higher educational status.  Out of 128 patients, 73 (57.03%) patients having LPR owned academic degree or higher education. The prevalence of LPR is less among people who could not complete their high school education.
  • 49.  The two most troublesome symptom as mentioned by the patients were foreign body sensation throat/ globus sensation followed by hoarseness of voice, found in 121(94.53%) and 117 (91.41%) patients, respectively.  Other complains include : throat clearing in 11(88.28%), cough after eating/lying down in 102 (79.69%), annoying cough in 100 (78.13%), excess mucus or post nasal discharge in 92 (71.88%), heartburn in 72 (56.25%) patients.  Least commonly mentioned symptoms were breathing difficulty and difficulty in swallowing, observed by 20 (15.63%) and 22 (17.19%) patients of laryngopharyngeal reflux, respectively .
  • 50. Prevalence of various symptoms in LPR suspected patients
  • 51. Endoscopic findings among patients with laryngopharyngeal reflux before and after Proton Pump Inhibitor treatment
  • 52. The laryngoscopic examination showed that the most common sign of laryngeal inflammation observed in our study population was erythema which was found in 121 (94.53%) patients followed by thick laryngeal mucosa in 116 (90.63%) patients. Other signs observed were: posterior commissure hypertrophy in 113 (88.28%), vocal fold oedema in 95(74.22%), diffuse laryngeal oedema in 90 (70.31%), ventricular oedema in 77 (60.16%) & subglottic oedema in 40 (31.25%). The least commonly seen sign on laryngeal endoscopy was granuloma, found in 18 (14.06%) patients.
  • 53. Endoscopic findings among patients with LPR before and after Proton Pump Inhibitor treatment
  • 54. The overall effect of PPI on all the symptoms of LPR included in RSI is statistically significant except on the swallowing difficulty where improvement was there but not statistically significant at p<0.01. The study elucidated that PPI are effective in relieving the symptoms of LPR patients . Improvement of laryngeal symptoms after the PPI treatment
  • 56. The final data interpretation was for the comparison of RSI and RFS before and after the PPI treatment and the corelation between RSI & RFS : Using Wilcoxon signed rank test, z -9.817; p value <0.0001 The RSI ≥13 was our inclusion criteria, therefore all of the 128 patients showed RSI ≥ 13. But after the PPI treatment, RSI improved significantly in all 128 patients. The average RSI before treatment was 20 which dropped down significantly to average of 4 after PPI treatment and the result was significant at p<0.01 Comparison between RSI before and after PPI treatment
  • 57.  The study showed that average RFS before PPI treatment was 12 and after the PPI treatment it improved significantly to average of 3.594 ~4.  The result was significant at p<0.01. Before initiation of treatment, all of 128 patients had RFS ≥ 7 and this no. decreased substantially after the treatment to RFS < 7 in 109 patients. Comparison between RFS before and after PPI treatment
  • 58. Evaluating Pearson correlation coefficient, the value of R = 0.3717 ; R2 = 0.1382 showing positive correlation between the RSI & RFS. The result signifies that RSI & RFS are related to each other and any change in the RSI will affect the value of RFI and vice versa. Also p=0.000016 so the result is significant at p<0.01. Correlation between RSI and RFS
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