CAROL DAVILA UNIVERSITY OF MEDICINE AND PHARMACY. [603238]

“CAROL DAVILA” UNIVERSITY OF MEDICINE AND PHARMACY.
FACULTY OF MEDICINE.

DIPLOMA THESIS
“Minimal invasive method for GERD”

SCIENTIFIC CO ORDINATOR:
PROFESSOR M. BEURAN MD, PHD , FACS
TUTOR:
SENIOR LECTURER BOGDAN GASPAR, MD, PHD

GRADUATE: Namarna Zina

BUCHAREST 2018.

Table of contents

Page
➢ Introduction 1

➢ General Part 2

I. ANATOMY of the esophagus

• 1.1 Gross anatomy 3
• 1.2 Relationships of the esophagus 5
• 1.3 Arterial Blood Supply 6
• 1.4 Venous drainage 7
• 1.5 Lymphatic drainage 8
• 1.6 Nerve supply 9
• 1.7 Micro scopic anatomy 10
• 1.8 Pathophysiologic variants 11

II..ANATOMY of the stomach

• 2.1 Gross anatomy 12
• 2.2 Relationships of the stomach 13
• 2.3 Arterial Blood Supply 14
• 2.4 Venous drainage 16
• 2.5 Lymphatic drainage 17

• 2.6 Nerve supply 18
• 2.7 Anatomy on diagnostic imaging 21
• 2.8 Endoscopic anatomy 21
• 2.9 Physiological anatomy 21
• 2.10 Microscopic anatomy 21
• 2.11 Wall layers on ultrasonography 23
• 2.12 Pathophysiologic variants 23

III.Semiology

• 3.1 Definition 24
• 3,2 Epidemiology 28
• 3.3 Etiology 28
• 3.4 Risk factors for GERD 29
• 3.5 Signs and Symptoms 33
• 3.6 Diagnosis 34
• 3.7 Minimally invasive approach used to treat GERD 39
• 3.8 Treatment 40

IV.Surgery
• 4.1 Surgical intervention 42
• 4.2 Surgical technique 42

• 4.3 Postoperative care 48
• 4.4 Complications 48
• 4.5 Differential diagnosis 49
• 4.6 Prevention 50

➢ Special Part

• 5.1 Introduction 52
• 5.2 Aim of study 52
• 5.3 Patient selection 53
• 5.4 Inclusion Criteria of the Study 54
• 5.5 Exclusion Criteria of the St udy 54
• 5.6 Observational results 55
• 5.7 Result summary 73

➢ Conclusions 74

➢ Bibliograph y 75

1

INTRODUCTION

Surgery is an ancient medical specialty that uses manual and instrumental techniques on a
patient to investigate and/or treat a pathological condition :a diseases or injury , to help improve
the function of the body or the appearance .

Nowadays, surgery has become the result of centuries of consequent victories over
death. The procedures have not always been the safest or the cleanest ,both for the
surgeon and the patient .Over the years, errors tend to be solved in multiple ways and
now, su rgeons are able to perform a majority of surgeries from multiple fields of
medicine in clean, safe and organized environments. Due to proper surgical techniques
and methods the complications post surgery have decreased tremendously and will keep
decreasing .

Having always an interested in activities that required me to work w ith my hands, slow and
steady, I always wanted to help others but in a way that was other than just words . I enjoyed
being able to see a lot of patients in many hospitals with their pathologies, and after the surgery
being taken, to see the patients recovering (that was the best feeling because I really saw how
their quality of life was improved).Also, seeing the differences between taking long -term
treatment and the laparoscopic t echniques used nowadays, made me think about studying them
more.

This study is to present the advantages of a non -invasive procedure for the patients
suffering from GERD( Gastro esophageal reflux disease). Choosing GERD was not a
hard decision, becau se a lot of people are suffering from it. I will present the the subject
by discussing the procedure through a retrospect ive study that will be done at t he
Emergency Hospital Floreasca under the supervision of my professor Dr. Gaspar
Bogdan.

2

GENERAL PART

3
I. Anatomy of the Esophagus

1.1.GROSS ANATOMY
The esophagus is a 25 -cm long muscular tube that makes the connection between pharynx and
stomach .[1](Fig.1) The length of the esophagus differs: at birth is 8 to 10 cm and measures about
19 cm at the age of 15 years.
The esophagus extends from the lower border of the cricoid cartilage (located at the level of the
sixth cervical vertebra) to the cardiac orifice of the stomach at the side of the body of the 11th
thoracic vertebra. The upper limit in the newborn infant is at the level of the fourth or fifth
cervical vertebra, and it ends much higher, at the level of the ninth thoracic vertebr a. [2, 3]

Fig.1 Human Esop hagus
Source: https://thoracickey.com/esophagus/#s0730
In its vertical course, in the coronal plane , the esophagus has 2 gentle curves. The first curve
begins a below the commencement of the esophagus and inclines to the left as far as the root of
the neck and returns to the midline at the level of fifth thoracic vertebra. The second curve to the

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left is formed as the esophagus bends to cross the descending thoracic aorta, before it pierces the
diaphragm. The esophagus also has anteroposterior curvatures that correspond to the curvatures
of the cervical and thoracic part of the vertebral column.[1, 2]
The esophagus, in its vertical co urse , has 3 constrictions, as follows:
• The first constriction is at 15 cm from the upper incisor teeth, where the esophagus
begins at the cricopharyngeal sphincter; this is the portion that corresponds to the sixth
cervical vertebra of the esophagus and it is narrowest one
• The second constriction is at 23 cm from the upper incisor teeth, where it is crossed by
left main bronchus and the aortic arch (Fig.2)
• The third constriction is at 40 cm from the upper incisor teeth, where it pierces the
diaphragm; at this level is situated the lower esophageal sphincter (LES)

Fig.2 Esophagus in Situ
Source: Atlas of Human Anatomy,Frank H. Netter

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These measurements are important for endoscopy and endoscopic surgeries of the esophagus.

1.2.RELATIONSHIPS OF THE ESOPHAGUS
The esophagus has been subdivided into 3 portions, as follows:
• The cervical portion is from the cricopharyngeus to the suprasternal notch
• The thoracic po rtion is from the suprasternal notch to the diaphragm
• The abdominal portion is from the diaphragm to the cardiac portion of the stomach .

The relationships of the cervical, thoracic, and abdominal esophagus are described below:

¤ The cervical part of the esophagus
The trachea is anterior to the esophagus and the connection between them is made by a loose
connective tissue. Posteriorly, there are prevertebral fascia and prevertebral muscles covering
the bodies of 6th, 7th, and 8th cervic al vertebra. The thoracic duct is on the le ft side at the level of
the 6th cervical vertebra. The carotid sheath with its contents and lower poles of the lateral lobes
of gland are in lateral relation to the esophagus.

¤The thoracic part of the esophagus
The esop hagus is in the superior mediastinum and lies between the trachea and vertebral
column. On its course, way down , the esophagus passes behind the aortic arch, and, at the level
of T4/T5 intervertebral discs, it enters in the posterior mediastinum. The thoracic duct is on the
left side, and the left recurrent laryngeal nerve is in the left tracheoesophageal groove. Laterally,
on the left side, there are the left subclavian artery and the aorta; on the right side, it is the
azygos vein.
Anteriorly, the esophagus is related to the trachea, right pulmonary artery, left bronchus,
pericardium with left atrium, and diaphragm. Posteriorly, the esophagus has the vertebral

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column, right posterior intercostal arteries, thoracic duct, thoracic part of the aorta, and
diaphragm. In the posterior mediastinum, the esophagus is related to the descending thoracic
aorta, left mediastinal pleura, azygos vein, and cardiac and pulmonary plexus.

¤The abdominal part of the esophagus
The esophagus passes through the right crus of the diaphragm. In its abdominal course, it is
covered with the peritoneum of the greater sac on its left side and anteriorly , and on the right
side it is covered with the lesser sac pe ritoneum. On the posterior surface of the left lobe of the
liver, it comes to lie in the esophageal groove and curves sharply to the left to join the stomach at
the cardia. The right border continues into the lesser curvature, whereas the cardiac notch
separates the left border f rom the fundus of the stomach .[2]

1.3. ARTERIAL BLOOD SUPPLY

The arterial blood supply depends on the portion of the esophagus(Fig.3) :
• The cervical portion is supplied by the inferior thyroid artery
• The thoracic portion is supplied by bronchial and esophageal branches of the thoracic
aorta
• The abdominal portion is supplied by the ascending branches of the left ga stric and left
phrenic arteries.[1]

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Fig.3 Arterial blood supply of the esophagus
Source: https://thoracickey.com/esophagus/#s0730

1.4.VENOUS DRAINAGE
Venous blood from the esophagus drains into a submucosal plexus. From the submucosal plexus,
blood drains to the periesophageal venous plexus. Esophageal veins arise from this plexus and
drain in a segmental way similar to the arterial supply, as follows (Fig.4) :
• From the cervical esophagus, veins drain into the inferior thyroid vein

• From the thoracic esophagus, veins drain into the azygos veins, intercostal, hemiazygos,
and bronchial veins

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• From the abdominal portion, esophagus veins drain into the left gastric vein; a tributary
of the portal system is the left gastric vein . [1, 2]

Fig.4 Venous drainage of the esophagus
Source: https://thoracickey.com/esophagus/#s0730

1.5.LYMPHATIC DRAINAGE OF THE ESOPHAGUS

The esophagus has an extensive submucosal lymphatic system.[2] The esophagus has 2 types of
lymphatic vessels. A plexus of large vessels is in the mucous membrane, and it is continuous
above with the mucosal lymphatic vessels of pharynx and below with mucosal lymphatic vessels
of gastric mucosa. The second plexus of finer vessels is in the muscular coat. Efferent vessels
from the cervical part dr ain into the deep cervical nodes. Vessels from the thoracic part drain to

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the posterior mediastinal nodes and from the abdominal part drain to the left gastric nodes .The
thoracic duct has some vessels that may pass directly to it.[1, 2]
Esophageal lymphatics are densely interconnect ed and l ymphatic drainage of the esophagus
contains little barrier to spread . Esophagus carcinoma can spread through the length of the
esophagus via lymphatics and may also have nodal involvement several centimeters away from
the primary lesion . [3]

1.6. NERVE SUPPLY

Recurrent laryngeal branches of the nerve supply (in the upper third of the esophagus )the striated
muscle, and cell bodies for these fibers are situated in the nucleus ambiguus in its rostral part .
The parasympathetic supply to the nonstriated muscle and cell bodies for these fibers are
situated in the dorsal nucleus of vagus. These fibers reach the esophagus through the vagus and
its recurrent laryngeal branches. They synapse (in the esophagus wall ) in the ganglia of
myenteric plexus (Auerbach) and s ubmucosal plexus (Meissner) . The myenteric is situated
between the inner circular and outer longitudinal muscle fibers. From these plexuses,
postganglionic fibers emerge to innervate the smooth muscle fibers within the walls of the
esophagus [2] and the mucous glands.

Vasomotor sympathetic fibers (that supply the esophagus ) arise from the upper 4 -6 thoracic
spinal cord segments. Fibers from the upper ganglia pass to the middle and inferior cervical
ganglia and synapse on postganglionic neurons. The axons of these ne urons innervate the vessels
of both cervical and upper thoracic esophagus .Postsynaptic fibers (from the lower ganglia ) pass
to the esophageal plexus to innervate the distal esophagus. Afferent visceral pain fibers travel via
the sympathetic fibers to the first 4 segments of the thoracic spinal cord.[1]

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1.7. MICROSCOPIC ANATOMY
Histologically, the esophagus has the following 4 concentric layers (Fig.5) :
• Mucosal layer
• Submucosal layer
• Muscular layer
• Adventitial layer

• Fig.5. Layers of the esophagus • Fig.6 Z Line
Source: https://thoracickey.com/esophagus/#s0730

The innermost layer is the mucosa and is formed by a nonkeratinizing stratified squamous
epithelium . At the gastroesophageal junction, mucosal epithelium changes from squamous cell
epithelium to columnar cell epithelium. This junction has been named the squamocolumnar
junction or "Z line". (Fig.6)[2, 3]
The second layer is the submucosa, and it connects the muscular coat and the mucous membrane.
This layer contains the esophageal glands , blood vessels, and the submuco sal (Meissner) nerve
plexus .[2, 3]

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The third layer is formed by circular and longitudinal muscle fibers. The longitudinal layer is
thicker than the circular layer :
• Inner circular muscle fibers: These fibers are continuous inferiorly wi th oblique fibers of
the stomach and superiorly with the fibers of the cricopharyngeal part of the inferior
constrictor [2]
• Outer longitudinal muscle fibers: The longitudinal muscle fibers form a continuous coat
around the whole of the esophagus ( except posterosuperiorly ), 3-4 cm below the cricoid
cartilage; here, they diverge as 2 fascicles that are going obliquely to the anterior aspect
of the esophagus [1, 2]
The proximal one -third of the esophagus if formed by striated muscle. In the distal portion
predominate s smooth muscle . [3]
The fourth layer i s formed by external adventitia of irregular, dense connective tissue containing
a lot of elastic fibers.

1.8 PATHOPHYSIOLOGIC VARIANTS
The most common congenital anomalies of the esophagus are esophageal tracheoesophageal
fistula and atresia (Fig.7) . The cause of esophageal atresia is considered to be a failure of the
esophageal endoderm to proliferate rapidly during the fifth week to keep up with the embryo
elongation. The cause for tracheoesophageal fistula and the reason why the 2 defects are usu ally
found together is related to esophageal development, to the fact that the respiratory diverticulum
buds anteriorly from the cranial foregut . [4]

Fig.7 Esophageal atresia
Source : Essential Neonatal Medicine, sixth edition.

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II.Anatomy of the Stomach

2.1. GROSS ANATOMY
The stomach is the first intra -abdominal part of the digestive or gastrointe stinal (GI) tract. It is a
highly vascular and muscular, bag -shaped organ (Fig.8) that is distensible depending on the build
and posture of the person and the state of fullness of the organ and may take varying shapes . The
stomach lies in the left upper quadrant of the abdomen . [5, 6]
The thoracic esophagus enters in the abdomen via the esophageal hiatus of the diaphragm at the
level of T10. The abdominal portion of the esophagus has a small i ntra-abdominal length(2 -3
cm). The cardia (esophagogastric junction ), lies below the diaphragm to the left of the midline at
the T11 level.
The cardiac notch is the acute angle between the fundus of the stomach and the left border of
the abdominal esophagu s, the fundus is the part of stomach above a horizontal line drawn from
the cardia. The body (corpus) of the stomach leads to the pyloric antrum (at the incisura
angularis). The pyloric antrum narrows toward the right to become the pyloric canal, that is
surrounded by the pyloric sphincter, which joins the duodenum at the L1 level (transpyloric
plane).

Fig.8 Stomach
Source:http://www.edoctoronline.com/medical –
atlas.asp?c=4&id=22135&m=1&p=10&cid=1064&s=

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2.2 RELATIONSHIPS OF THE STOMACH

The anterior surface of stomach is related to the the anterior abdominal wall ,to the left lobe
(segments II, III and IV) of the liver, and to the distal transverse colon. The posterior surface of
the stomach is related to the the spleen ,to the left kidney (and adrenal) ,to the left
hemidiaphragm and and to the pancreas (stomach bed).

The omental bursa (lesser sac) lies behind the stomach ,in front of the pancreas; it communicates
via the omental (epiploic) foramen (of Winslow) with the greater sac (main peritoneal cavity)
behind the hepatoduodenal ligament (HDL).

The greater curvature (that is convex) of the stomach begins at the left of th e cardia and it goes
from the fundus along the left border of the corpus of the stomach and the inferior border of the
pylorus. The lesser curvature (that is concave) starts at the right of the cardia as a continuation of
the right border of the abdominal e sophagus and runs along the right border of the body of the
stomach (for a short distance) and the superior border of the pylorus. The junction of the
horizontal and vertical parts of the lesser curvature is called incisura angularis. Lesser curvature
is much shorter in length than the greater curvature.

The first part of the duodenum and t he stomach are attached to the spleen by the
gastrosplenic/gastrolienal ligament containing short gastric vessels, to the liver by the
hepatogastric ligament containing left and right gastric vessels, to the left hemidiaphragm by the
gastrophrenic ligament, and to the transverse colon by the gastrocolic ligament (part of the
greater omentum) containing omental (epiploic ) vessels. Few peritoneal bands may be present
between the anterior surface of the pancreas and the posterior surface of the stomach .

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2.3 ARTERIAL BLOOD SUPPLY

The arterial blood supply of the stomach has a lot of branches.(Fig. 9)
The celiac trunk (axis) starts from the anterior surface of the abdominal aorta at the level of L1.
It has a short length (about 1 cm) and trifurcates into the splenic artery, the common hepatic
artery (CHA), and the left gastric artery (LGA).

The LGA runs toward the lesser curvature o f the stomach and divides into a descending branch
(supplying the proximal stomach) and an ascending branch (supplying the abdominal
esopha gus). The CHA runs toward the right on the superior border of the pancreas and gives off
the gastroduodenal artery (GD A), which runs down behind the first part of the duodenum. After
this, the CHA continues as the proper hepatic artery.

The right gastric artery (RGA), a branch from the common or proper hepatic artery, runs along
the lesser curvature from right to left an d joins the descending branch of the LGA to form an
arcade between the 2 leaves of peritoneum of the lesser omentum, along the lesser curvature.
This arcade gives off multiple small arteries to the corpus of the stomach. The GDA gives off the
PSPDA (posterior superior pancreaticoduodenal artery) and then divides into the anterior superior
pancreaticoduodenal artery (ASPDA)and the right gastro -omental (gastroepiploic) artery
(RGEA); it also gives off the small supraduodenal artery (of Wilkie). The RGEA runs from right
to left , along the greater curvature.

The splenic artery runs toward the left on the superior border of the distal body and tail of
pancreas and gives off the left gastro -epiploic (gastro -omental) artery (LGEA), which runs along
the great er curvature from left to right and joins the RGEA to form an arcade between the two
leaves of peritoneum of the greater omentum . This arcade gives off many small arteries to the
body of the stomach.

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The greater curvature arcade formed by the LGEA and the RGEA provides several omental
(epiploic) branches to supply the greater ome ntum. The splenic artery also gives off 3 -5 short
gastric arteries that run in the gastro -splenic (gastro -lienal) ligament and supply the gastric
fundus and the upper part of the gr eater curvature . Few small posterior gastric arteries may arise
from the splenic artery. The stomach has in its submucosa a rich network of vessels.

Fig 9. Arterial blood supply of the stomach
Source: http://academicdepartments.musc.edu/radiology/divisions/interventional/atlas/images/CH
AP18FIG31.jpg

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2.4 VENOUS DRAINAGE OF THE STOMACH
The left gastric (coronary) vein drains into the portal vein at its formation (by the union of the
splenic and superi or mesenteric veins). The right gastro -omental and right gastric veins drain into
the portal vein. The left gastro -omental vein drains into the splenic vein, as do the short gastric
veins. (Fig.10)
The pylorus is marked by a prepyloric vein (of Mayo), which lies on its anterior surface. The
gastrocolic trunk (GCT) of Henle lies at the junction of the small bowel mesentery and the
transverse mesocolon. It may drain branches from the middle colic, ASPDV (anterior superior
pancreaticoduodenal vein) and right gastro -omental veins.
The short gastric veins and arteries are sometimes referred to as the vasa brevia (short branches of
the splenic artery and vein that run to the greater curvature of the stomach).(Fig.11)

Fig.10 Venous drainage of the stomach
Source: https://medizzy.com/feed/778919?title=venous_drainage_of_stomach

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Fig 11. Blood supply of the stomach
Source: https://humananatomycharty.com/stomach -blood -supply/stomach -blood –
supply -stomach -and-its-blood -supply -picture -mbbs -medicine -humanity -first/

2.5. LYMPHATIC DRAINAGE OF THE STOMACH

Lymph nodes draining the stomach (Fig.12) are numbered and divided into 4 levels, as follows:
• Level I (perigastric lymph nodes) – Right paracardiac (1), left paracardiac (2), along
lesser curvature (3) along greater curvature (4), suprapyloric (5), infrapyloric (6)
• Level 2 – Along LGA (7), along CHA (8), along celiac axis (9), at splenic hilum (10),
along splenic artery (11)
• Level 3 – In hepato -duodenal ligament (12), behind duodenum and pancreas head (13), at
the root of small bowel mesentery (14)
• Level 4 – Mesocolic (15), paraaortic (16)

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The gastric lymph nodes consist of two sets, superior and inferior.
• The Superior Gastric Glands accompany the left gastric artery and are divisible into three
group s:
(a) upper, on the stem of the artery;
(b) lower, along the cardiac half of the lesser curvature of the
stomach ,accompanying the descending branches of the artery, between the two
layers of the lesser omentum ;
(c) paracardial outlying members of the gastric glands, disposed in a manner
comparable to a chain of beads around the neck of the stomach. They receive their
their efferents pass to the celiac group of preaortic lymph nodes and their
afferents from the stomach;
• The Inferior Gastric Glands , four to seven in number, lie along the pyloric half of the
greater curvature of the stomach ,between the two layers of the greater omentum .

Fig.12 Lymphatic drainage of the stomach
Source: https://www.123rf.com/photo_83150887_lymphatic -drainage -of-liver-lymph -and-
liver.html

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2.6 NERVE SUPPLY

The esophageal plexus of vagus nerves lies below the hila of the lungs, in the posterior
mediastinum. It divides into 2 vagal trunks that enter the abdomen along with the esophagus
through the esophageal hiatus in the left dome of diaphragm. The left vagus is in front of the
intra-abdominal esophagus and t he right (posterior) vagus is behind and to the right of the intra –
abdominal esophagus .

The right vagus gives off a posterior gastric branch, which traverses to the left and supplies the
fundus and cardia of the stomach . The right vagus gives off a celiac branch (Fig.13) (whic h
supplies the small and large bowel and the pancreas), and the left vagus gives off a hepatic
branch (which supplies the gallbladder and the liver).

After giving off the celiac and hepatic branches, respectively, the right and left vagal trunks
continue along the lesser curvature of the stomach (in close company with the vascular arcade
formed by the left and right gastric vessels) as the posterior and anterior gastric nerves of
Latarjet, which supply the antrum ,the pylorus and the corpus (body) of the s tomach .
Sympathetic nerve supply comes from celiac ganglia (T5 -T9).

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Fig.13. Autonomic innervation of stomach
Source:Atlas of Human Anatomy, Frank H. Neter

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2.7 ANATOMY ON DIAGNOSTIC IMAGING
The stomach and duodenum are evaluated radiologically with barium studies using fluoroscopy.
It should be known that on computed tomography (CT), the cardia is on a lower horizontal plane
than the dome of the fundus is.

2.8 ENDOSCOPIC ANATOMY
Cardia (eso phagogastric junction), incisura angularis, and pylorus are very well seen on upper GI
endoscopy (UGIE).

2.9 PHYSIOLOGICAL ANATOMY
Stomach is a reservoir; its size and shape changes from time to time depending on the volume of
its contents (food/fluid). The position and shape of the stomach also changes with the position of
the patient . A large J -shaped stomach can go as low down as into the pelvis.
Severe pain in any part of the body (eg, headache, ureteric colic due to stone) may give rise to
reflex vomiting and pyloro spasm .

2.10 MICROSCOPIC ANATOMY
The esophagus has nonkeratinized stratified squamous epithelium, which changes into columnar
epithelium in the stomach. The columnar cells in the stomach secrete mucin; the parietal
(oxyntic) cells in the body (corpus) of the stomach secrete acid (H+ ions) and intrinsic factor, the
G cells in the antrum secrete gastrin (which in turn acts on parietal cells)and the chief
(zymogenic) cells in the fundus secrete protein digesting pre -enzyme pepsinogen. (Fig. 14)
The mucosa which is the innermost lining of the stomach wall , consists of columnar epithelium,
muscularis mucosa and lamina propria . Submucosa contains the Meissner’s nerve plexus and a
rich network of blood vessels . The smooth muscles of the s tomach are arranged in 3 layers:
outer longitudinal , middl e circular (forms the pylorus) and inner oblique (unique to stomach) .
These muscles are supplied by the Auerbach’s nerve plexus .The stomach is covered by the

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serosa(visceral peritoneum) . Mucosa and submucosa are thrown into several longitudinal folds
called rugae. (Fig.15)

Fig.14 Stomach Histology
Source: http://histology.ro/Histology/ETG_files/3%20Epithelial_2_17.pdf

Fig.15 Layers of the stomach
Source: https://opentextbc.ca/anatomyandphysiology/chapter/23 -4-the-stomach/

23

The lower esophageal sphincter (LES), or gastroesophageal sphincter, is n ot a true (anatomic)
sphincter.T he pylorus is a true sphincter that consists of circular muscles.

2.11 WALL LAYERS ON ULTRASONOGRAPHY

Endoscopic ultrasonography (EUS) is a technical tool for evaluating stomach. An ultrasound
probe is mounted at the tip of an upper gastrointestinal endoscope, which is passed into the
stomach. The wall of the stomach is see n as 5 alternating layers, as follows:
• Mucosa (hyperechoic)
• Lamina propria (hypoechoic)
• Submucosa (hyperechoic)
• Muscularis propria (hypoechoic)
• Serosa (hyperechoic)
EUS is helpful for evaluation of gastric varices in portal hypertension and for the diagno sis and
staging of early gastric cancer .

2.12 PATHOPHYSIOLOGIC VARIANTS
Congenital hypertrophic pyloric stenosis seen in infants presents as pyloric obstruction at 2-4
weeks of life.

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III. SEMIOLOGY
3.1 DEFINITION

Gastroesophageal reflux disease (GERD) is a condition that is characterized by either a
dysfunctional lower esophageal sphincter (LES) or a weak that results in partially digested food
from the stomach to flow back into the esophagus, a process known as reflux.

Persistent GERD may lead to serious conditions, such as : esophageal damage, strictures
,severe esophagitis, Barrett's metaplasi a, and adenocarcinoma of the esophagus.
Gastroesophageal reflux disease is the most common gastrointestinal diagnosis recorded during
visits to outpatient clinics.[7]

GERD is considered to be “a condition which develops when the reflux of stomach
contents causes troublesome symptoms (i.e., at least two heartburn episodes per week) and/or
complications.”[8]

Many extraesophageal manifestations of the disease are well known , including la ryngitis
and cough (Table I ). With respect to the esophagus, the spectrum of injury includes esophagitis
(Fig. 1 6A), stricture (Fig. 1 6B), the development of columnar metaplasia in place of the normal
squamous epithelium (Barrett’s esophagus) (Fig. 1 6C), a nd adenocarcinoma (Fig. 1 6D).
Esophageal adenocarcinoma has a rising incidence.[9-11]

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Table I . Symptoms and Conditions Associated with Gastroesophageal Reflux Disease.
Esophageal syndromes
Symptoms with or without esophageal injury
Common symptoms: heartburn, regur gitation, dysphagia, chest pain
Less common symptoms: water brash (excessive salivation prompted by acid reflux),
odynophagia (pain with swallowing), subxiphoid pain, nausea
Injury (with or without esophageal symptoms)
Reflux esophagitis: n ecrosis of esophageal epithelium causing ulcers or erosions at or
immediately abov e the gastroesophageal junction
Barrett’s esophagus: endoscopically suspected and histologically confirmed meta plasia in
the distal esophagus
Esophageal adenocarcinoma
Stricture: a persistent luminal narrowing of the esophagus caused by reflux -induced
inflammation

Extraesophageal syndromes
Association with gastroesophageal reflux d isease established but good evi dence for
causation only when accompa nied by an esophageal syndrome
Asthma (reflux as a cofactor leading to poorly controlled disease)
Recurrent otitis media
Laryngitis (hoarseness, throat clearing): reflux usually a cofactor along with excessive
use of the voice, envir onmental irritants, and smoking
Erosion of dental enamel
Chronic cough
Proposed association with gastroesophageal reflux disease but neither associa tion nor
causation established
Idiopathic pulmonary fibrosis Pharyngitis
Sinusitis

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Fig.16 Spectrum of Esophageal Injury in Gastroesophageal Reflux Disease.
Gastroesophageal reflux is associated with esophagitis caused by erosions of the distal
esophageal mucosa (Panel A, arrows), distal esophageal stricture as a consequence of chronic
erosive esophagitis (Panel B, arrows), Barrett’s esophagus with columnar metaplasia of the
normal squamous epithelium (Panel C, arrows), and esophageal adenocarcinoma (Panel D,
arrow), shown here in a patient with Barrett’s esophagus (arrowheads).
Source: Gastroesophageal Reflux Disease, Peter J. Kahrilas, M.D., N Engl J Med
2008;359:1700 -7.

Esophagitis occurs when excessive reflux of pepsin and acid results in necrosis of surface
layers of esophageal mucosa, causing ulcers and erosions . For many patients the impaired
clearance of the refluxed gastric juice from the esophagus also contributes to the damage. Some
gastroesophageal reflux is normal (and relates to the ability to belch), but several factors may
predispose patients to pathologic reflux, including loss of esophageal peristaltic function , hiatus
hernia,[12,13] abdominal obesity,[13,14] lower es ophageal sphincter hypotension, increased
compliance of the hiatal canal,[15] delayed gastric emptying, gastric hypersecretory states,[16] and
overeating. Often multiple risk factors are present.
A consistent paradox is that gastro esophageal reflux disease has the imperfect correspondence
between symptoms attributed to the condition and endoscopic features of the disease.

27
Gastroesophageal reflux disease refers to the pathological symptoms and complications that
result from reflux. A number of physiologic barriers exist to prevent reflux from the stomach into
the lower esophagus, such as the angle of HIS , the length of the i ntra-abdominal esophagus and
the lower esophageal sphincter . In addition, many mechanisms are present to limit esophageal
injury, su ch as saliva and other enzymes and to minimize the amount of reflux in the esophagus,
such as esophageal peristalsis . The ad verse effects occur from the failure of one or more of these
factors. Transient lower esophageal sphincter relaxation is the most important pathophysiologic
mechanism leading to GERD. Esophageal atresia and congenital diaphragmatic hernia are some
congenit al anomalies that also increase the risk of GERD .
In normal digestion, the lower esophageal sphincter (LES) opens to allow food to pass into the
stomach and closes to prevent parts of food and acidic stomach juices from flowing back into the
esophagus. Gastroesophageal reflux occurs when LES pressure is lower than intragastric
pressure. Under normal circumstances a small amount of reflux occurs when LES pressures are
low with a swallow and during TLESR (transien t lower esophageal sphincter relaxation) , and
when increases in intraabdominal pressure or intragastric pressure overcome the
resting LES pressure.
The LES is an anatomically complex zone located at the gastro -esophageal junction, comprising
two components: the true LES, a segment of tonically contracted smooth muscle located in the
distal esophagus and the crural portion of the diaphragm. Both the diaphragm and the LES
contribute to gastro -esophageal sphinct er competence. Physiologically, relaxations of the LES,
prior to contractions of the esophagus, allow food to pass through into the stomach. In resting
conditions, LES maintains a high -pressure zone that is 15 -30 mmHg above intragastric pressures,
depending on individual variability.
The severity of GERD depends on the type and amount of fluid brought up from the stomach ,on the
neutralizing effect of saliva as well as on the LES dysfunction .

28
3.2 EPIDEMIOLOGY

Gastroesophageal reflux disease is a condition that appears when the reflux of gastric contents
causes troublesome symptoms or complications. GERD is responsible for some of the most
common symptoms and leads to a lot of presentation s for medical care. The prevalence of GERD
symptoms and the incidence of some of the complications have risen too much over the last few
decades, leading to an important economic impact. There are many potential explanations for
these rising trends. Symptoms of GERD seem to be more common now than 25 years ago.

The prevalence and incidence of GE RD was estimated fr om many studies which defined GE RD
as at least weekly heartbur n and/or acid regurgitation. Da ta on factors associated with GE RD
were also evaluated.
To est ablish the true prevalence of GE RD, a symptom threshold must be defined which
adequately selects for patients whose quality of life is impaired as a result of thei r disease.
Experience of heartburn at least twice weekly is thought to be sufficient to result in impaired
quality of life.[17]
A minority of patients with GERD have a constantly weak, low -pressure LES, which permits
reflux every time the pressure in the stomach exceeds the LES pressure. This occurs when LES
pressure is <6 mmHg [18]. A chronically decreased LES resting tone is associated with severe
esophagitis. Also, LES defects have been found in many patients with other GERD
complications, such as Barre tt’s esophagus and esophageal stricture.

3.3 ETIOLOGY
GERD is caused by a failure of the lower esophageal sphincter. In healthy patients, the
gastroesophageal junction cardia where the esophagus ente rs the stomach creates a valve
->lower esophageal sphincter that prevents food and stomach acid from traveling back into the
esophagus where they can cause inflammation of sensitive esophageal tissue and
heartburning. Factors that decrease LES tone include endogenous hormones ( progesterone in

29
pregnancy ,cholecystokinin ) medications ( calcium channel blockers ,nitrates, etc.), specific foods
like high -fat meals and chocolate, and usually habits like caffeine , alcohol and smoking .

There is positive , but sparse , data on the association between genetic factors and GERD. This
aspect w as discussed in many studies. For exa mple, a study of the St Thomas’ Adult UK Tw in
Registry proved that there is a significantly associa tion between GERD and parental family
history of reflux disease (odds ratio (OR) 1.46 (95% CI 1.22 –1.74)).[19] It also highlighted the
higher concordance in prevalence of GE RD in monozygotic over dizygotic twin pairs (pairwise
concordance: 27% v 15%, p = 0.001; casewise concordance: 42% v 26%, p<0.001) . The second
study Olmsted County demonstrated an important association between symptoms of GE RD and
disease of the esophagus or significa nt heartburn or stomach disease .[20]

3.4 RISK FACTORS FOR GERD

There is no clear association of gender or age with GERD symptoms, but white race ,
advancing age and male gender are associated with the risk of GERD complications. Reports of
the association between gender and GERD symptoms have yielded conflicting results, with some
suggesting the prevalence is greater in men ,[21,22,23 ]some of them suggesting it is greater in
women ,[24]and others explaining that there is no difference by gender.[25–27]
Many reports have suggested GERD symptoms are associated with age,[22–24,27 ] but
others have suggest ed no association.[25,26]In contrast, mortality from GERD is associated
with white race and male gender.[28] Esophageal adenocarcinoma is associated with advancing
age,male gender , and white race .[29] Many o bservational studies assessing the association
between GERD symptoms and behaviors need to be interpreted cautiously. Alcohol consumption
has been inversely associated with GERD symptoms in some surveys,[27,30,31 ] but other surveys
indicate that alcohol consumption actually worsens esophageal acid exposure.[32] Many studies
have demonstrated a positive association between GERD symptoms and smoking,[27,30,31 ] but
studies of smoking cessation did not demonstrate a benefit on GERD symptoms.[32] This may be
a result by an enduring effect of tobacco exposure on weakening the lower esophageal
sphincter.[33]

30
Obesity is a high risk factor for GERD and its complications, and may explain
some of the rise in prevalence of GERD symptoms and incidence of complications . Some of the
effect of obesity on GERD might be confounded by associated differences
in dietary patterns or physical activity. Bearing in mind the issues raised
previously regarding behavior on GERD symptoms, it seems that dietary patterns might partially
confound the association of obesity with GERD. For example, obese individuals are more likely
to consume large meals with high fat intake, which can promote GERD. GERD has been
positively associated with consumption of sweets ,fat ,chocolate, and salt, and inversely
associated with consumption of fruits and fiber.[27,31,34,35 ]Leisure exercise is also inversely
associated with the presence of GERD symptoms ..[27,30,31] However, physical activity at
work may be positively associated with GERD symptoms.[30] It should be known that
certain forms of physical activity (eg, weight lifting) might promote immediate GERD
events.[36,37]
Infection with Helicobacter pylori is considered to be protective against esophageal
adenocarcinoma.[38] Initial reports also suggested that eradication of H pylori was
associated with the subsequent development of GERD.[39,40] It was thought
that H pylori led to a decrease in gastric acid production, and prevented GERD in people who
would otherwise be predisposed.[41] A meta -analysis of trials of H pylori eradication found that
there was no such increased risk of GERD symptoms after eradication of H pylori.[42] In
some studies, there has been an inverse association of H pylori with erosive esophagitis or
GERD symptoms, b ut the effect seems to be strongest in the Far East, where H pylori infection is
more commonly associated with corpus atrophy than in Western countries.[43]Antral -predominant
gastritis can be associated with an increase in gastric acid production and is m ore common in
Western countries .[44,45] In a study of older American men, it was recently confirmed an inverse
association between H pylori and erosive esophagitis and Barrett’s esophagus but could
not detect such an association with GERD symptoms.[46] There may be many other mechanisms
by which H pylori protects against Barrett’s esophagus ,erosive esophagitis, and esophageal
adenocarcinoma independent of any effect on GERD. GERD is associated with other medical
conditions. Most individuals with GERD symptoms do not present to a physician for their
symptoms. Those who do present are more likely to have depression, anxiety, irritable bowel
syndrome, somatization, and obsessing personalities.[47,48] GERD has also been associated with

31
respiratory disease s, including chronic obstructive pulmonary disease , asthma, interstitial
lung disease, and sleep apnea.[49–51]In each of these respiratory diseases, the initial work is
focused on how GERD might promote the respiratory complication and it seems that the
predominant direction of the effect is actually from asthma on GERD.[52] Further work is needed
to understand which direction the effect is with interstitial lung disease and chronic obstructive
pulmonary disease.
Sleep apnea represents is a special case. It has long been understood that GERD can
interfere with sleep, and that nocturnal symptoms increase the risk for complications.
It is clear that sleep disturbance of any sort can worsen GERD symptoms due to the increasing
esophageal sensi tivity to acid.[53] Therefore, in addition to its mechanical effect promoting
GERD, sleep apnea might promote esophageal hypersensitivity through sleep deprivation.

Factors that can contribute to GERD:
• Hiatal hernia , (Fig.17) which increases the likelihood of GERD due to mechanical and
motility factors.

• Fig.17. The changes in Hiatal Hernia
Source: http://hiatusherniainfo.blogspot.com/2012/03/signs -symptoms -of-hiatus -hernia.html

32

• Obesity : increasing body mass index is associated with more severe GERD.
• Zollinger -Ellison syndrom e, which can be present with increased gastric acidity due
to gastri n production.
• A high blood calcium level, which can increase gastrin production, leading to increased
acidity.
• Scleroderma and systemic sclerosis , which can feature esophageal dysmotility.
• The use of medicines such as prednisolone .
• Visceroptosis or Glénard syndrome, in which the stomach has sunk in the abdomen upsetting
the motility and acid secretion of the stomach.

GERD has been linked to a variety of respirator y and laryngeal complaints such as asthma ,
chronic cough , laryngitis , pulmonary fibrosis , earache , even when not clinically apparen t. These
atypical manifestations of GERD are commonly referred to as extraesophageal reflux disease
(EERD) or as laryngopharyngeal reflux (LPR) .

Factors that have been linked with GERD, but not conclusively:
• Obstructive sleep apnea
• Gallstones , which can impede the flow of bile into the duodenum , which can
affect the ability to neutralize gastric acid
• H. pylori infection: The eradication of H. pylori can lead to an increase in acid
secretion which attribute to GERD.

33
3.5 SIGNS AND SYMPTOMS
Gastroesophageal reflux disease (GERD) is defined as mucosal damage or symptoms produced
by the abnormal reflux of gastric contents into the esophagus or beyond, into the lung or oral
cavity (including larynx).
The main symptom of GERD is heartburn. Heartburn is discomfort felt behind the breastbone as
a burning sensation. It tends to get worse if the person lies down or bends over and also after
eating food.
However, not all people with GERD experience heartburn, and there are other possible
symptoms:
• nausea or vomiting
• Chest pain angina like
• respiratory and laryngeal symptoms:
1. Chronic cough
2. Hoarseness
3. Asthma worsening
4. sleep disturbances
• odynophagia pain within swallowing
• dysphagia difficulty within swallowing
• epigastric pain
• sensation of a lump in your throat

34
3.6 DIAGNOSIS

The diagnosis of gastroesophageal reflux disease is usually made on the basis of the history of
symptoms given by the patient to their doctor. Acid reflux is a common condition and not all of
the patients with symptoms require investigation. This is fortu nate because there is no
inexpensive definitive medical investigation f or reflux disease, apart from the empirical trial of
treatment with a PPI medication.
Specialists in gastro enterology have found that there is a correlation between symptoms and
severity of disease. This means that the majority of patients can be diagnosed confidently on the
basis of their history and possibly a trial of medication .It is also important to follow a GERD
diet.
A potential cardiac cause of the presenting symptoms sho uld always be prioritized. Using
endoscopy , the endoscopist should have a low threshold for obtaining specimens from
esophageal or gastric biopsy to detect alternative diagnoses, such as Helicobacter pylori gastritis
and eosinophilic esophagitis. Although endoscopy is the primary test in patients whose condition
is resistant to empirical therapy, its yield in this setting is low because of the poor correlation
between esophagitis and symptoms of gastroesophageal re flux disease, the likelihood that
preexisti ng esophagitis may have resolved with previous therapy, and the poor sensitivity for
detecting motility disorders. Physiological testing is not routinely needed but can be very helpful
in selected patients because it detects subtle motility disorders (esophageal manometry),
demonstrating abnormal exposure to esophageal acid in the absence of esophagitis (ambulatory
pH monitoring), or most recently, both quantifying exposure to esophageal acid and identifying
reflux events reg ardless of acidic content t o assess correlations with symp toms (combined
impedance –pH monitoring).

Empirical trial of acid suppression
The simplest way of making a diagnosis of GERD and assessing its relation to symptoms is the
empirical trial of acid suppression. Compared with other tests that only suggest an association
(e.g., esophagitis at endoscopy or positive symptom index on pH testing), the r esponse to anti –

35
reflux therapy can show a cause -and-effect relationship between symptoms and GERD.
Therefore, this has become the initial first test used in patients with classical or atypical
heartburn symptoms without having “alarm” complaints.
The popu larity of this method has been helped greatly by the discovery of the very effective
proton pump inhibitors (PPIs), which, unlike the histamine H2 receptor antagonists (HRAs), are
able to dramatically reduce the amount of acid reflux into the esophagus. Sy mptoms usually
respond in 7 –14 days with a trial of PPI’s. It is very safe to assume a diagnosis of GERD if
symptoms disappear with therapy and then return when the medication is stopped. A positive
response has been defined as at least a 50% improvement in acid reflux symptoms. Also,
empirical trials using a 2 -4 month regimen of PPIs taken twice a day also are commonly used in
patients with suspected GERD -associated asthma and reflux complaints which are related to the
nose, ear, and throat.
For diagnosing acid reflux disease ,an empirical trial of PPIs has a great many advantages. The
test is easy to perform, and is relatively inexpensive. It is also available to all physicians and
family doctors, and can avoid needless procedures and investigations. When s ymptoms of
gastroesophageal reflux disease are typical a nd the patient responds to therapy, there is no need
for diagnostic tests. The usual reasons prompting diagnostic testing are to avert misdiagnosis, to
evaluate treatment failures and to identify any complications (including stricture,
adenocarcinom a and Barrett’s metaplasia) . Important alternative diagnoses to consi der include
gastric or esophageal cancer , peptic ulcer disease, coronary artery disease, gallbladder disease ,
esophageal motility disorders, and eosinophilic, pill or infectious esophagitis.

From a practical perspective, there are two kinds of patients: those with atypical symptoms
(laryngeal, pulmonary, painful syndromes, etc.) and those with ty pical symptoms of reflux
(heartburn and regurgitation) . In the second group of patients, the strategy is to diagnose and
quantify (something that is probably not needed if only medical therapy is considered) the
presence of abnormal gastroesophageal (GE) re flux. In addition, the preo perative evaluation
should identify any additional pathology of the esophagus or stomach ,to define the anatomy of

36
the foregut, to and determine the quality of esophageal motility. There are routinely perform ed
manometry, upper tract endoscopy, an upper gas trointestinal series, and 24 -hour pH monitori ng
on each patient prior to sur gical therapy. In patients with atypical symptoms, one must not only
demonstr ate the presence of abnormal re flux but to correlate reflux and the symptom in question.

Patients with typical symptoms

Endoscopy can conf irm the diagnosis of GERD by de tecting Barrett’s esophagus or
esophagitis. Esophagitis is an indicator of severity and is present in only half of patients with
symptomatic reflux. The presence of esophagitis while a patient is on appropriate acid
suppression, is a strong indic ation for surgi cal therapy. It is not always possible to diagnose
Barrett’s esophagus by gross inspection alone, and the presence and quality of dysplasia or
metaplasia have a significant impact on the indication for operation. A biopsy of the
cardioesophageal junc tion, of the distal e sophagus, or both should al ways be performed.
Endoscopy can change the operative strategy and detect other foregut lesions that may ex plain
the patient’s symptoms.

An upper gastrointestinal series provides the position of the gastroesophageal GE junction and
its relations to the diaphragmatic hiatus. It identifies the presence of short esophagus or a
paraesophageal hernia, which may affect the surgical strategy and helps orient the surgeon to any
unusual intraoperative anatomi c findings. When spontaneous re flux is detected, it almo st always
correlates with abnor mal reflux.

Manometry provides information about the lower esophageal sphincter (LES ) pressure, as well
as the effectiveness and quality of esophageal peristalsis. A LES pressure ,10 mm Hg is almost
always associated with a defective valve mechanism and abnormal reflux.[54] Most operations for
reflux, create some restriction across the GE junction. Because of this, an assessment of the
effec tiveness of peristalsis has tra ditionally been an importan t part of the preoperative
evaluation. We have recommended in the past that patients with low -amplitude peristalsis (,30
mm Hg ) should un dergo partial fundoplication.[55] Because it is known that defective peristal sis

37
is often caused by GERD, defective peristalsis is now improved when abnormal reflux is
controlled, and because a total fundoplication is the most effective way to control reflux. Nissen
fundopl ication di d not increase the in cidence of dysphagia postoperatively.[56] In patients with
aperistalsis, however, it is still recommend the use of a partial (Toupet) fundoplication.

Barium esophagram
The barium meal ( esophagram) is a n easily available , cheap, and non-invasive test which
involves the patient swallowing a drink of bari um and then having a series of X -ray pictures
taken. This test is good at showing structural or physical narrowing of the esophagus and in
making a diagnosis of a hiatus hernia. It can show up a hiatus hernia and it can also give an idea
of the reducibility of a hiatus hernia. Other conditions which may show up only on an
esophagram are esophageal webs, Schatzki rings, or minimally narrowed peptic strictu res. These
can be missed by endos copy, which may not adequately distend the esophagus. These subtle
narrowings can be diagnosed more clearly by the addition of a marshmallow along with the
barium liquid or a 13-mm radio opaque pill. Suggesting the patient a prone oblique position
during swallows of barium, the barium esophagram will also allow demonstrate peristalsis
clearly. This is a useful test before an operation to show up a weak esophageal pump.
The ability of a esophagram or a barium mea l to make a diagnosis of esophagitis varies greatly.
The sensitivity for diagnosing severe or moderate esophagitis is 79% –100%, and mild
esophagitis is usually missed. Barium testing is also not good at showing up th e presence of
Barrett esophagus . There a re various ways of indicating stress reflux. These include: the
Valsalva maneuver, coughing, leg lifting, or t he water -siphon test. T hese tests may improve the
sensitivity of the barium esophagram, but it is also argued that they decrease its specificity i n
making a diagnosis of GERD.

Twenty -four-hour pH monitoring is the gold standard for defining and quantifying reflux.[57,58]
It determines whether the patient’s symptoms are associated with episodes of reflux, it confirms
the di agnosis of GERD, and it quantifies reflux severity.[59] The results from the pH monitoring

38
also serve as a baseline to compare with postoperative studies in patients with p ersistent
symptoms after antire flux operations.

Patients with atypical symptoms

It has been recognized that many atypical symp toms, such as asthma ,chest pain, laryngitis, and
cough, may be caused by abnorm al reflux. The evaluation of these patients is usually the same as
discussed above but with other studies more specific to the airway.

Standard 24 -hour pH monitoring in patients with airway disease reveals in the proximal
esoph agus, more acid exposure ,[60] but this finding is still nonspecific to prove a causal rel ation
for most of the patients. It has been demonstrated that a temporal relation between atypical
symptoms, such as cough and chest pain, is a good predictor of symptom response to therapy.
We perform pharyngeal pH monitor ing in patients with respiratory symptoms. The presence of
acid in the phary nx is a go od predictor of response to med ical[61] and surgical[62] antireflux
therapy.

The presence of lesions such as ulcer ation, nodularity, erythema, or granuloma is often
suggestive of reflux, but such lesions are not specific for reflux -induced injury.[63] Belafsky and
Koufman[64] quantified and grouped many of these findings into a scoring system. They were
able to show that the score imp roves with medical therapy, sug gesting that t heir system is a
promising tool.Laryngoscopy may as sist in makin g the diagnosis but should not stand alone.
Adding a biopsy of the laryngeal tissue does not help, and, in fact, the findings can rarely be
differentiated from those of normal subjects .[65] The response of respiratory symptoms to medical
antireflux therapy may help d etermine their relation to reflux.

The decision to operate on a patient with atypical symptoms should be made with as much
information as possible about the objec tive evid ence of airway exposure to acid and character of
the symptoms.

39

3.7 MIN IMALLY INVASIVE APPROACH USED TO TREAT GERD

• Radiofrequency energy: The Stretta procedure (Fig.18 ) administers radiofrequency (RF)
energy via endoscopic needles that are placed in the tissues surrounding the lower
esophageal sphincter. The RF energy is creating thermal lesions heating this neighboring
tissue. Submucosal scarring forms as the lesions heal, causing shrinkage and tightening
around the LES. These changes to the esophageal sphincter reduce acid reflux by restoring
the natural barrier f unctio n of the LES, and also reduces the spontaneous regurgitation
caused by transient relaxation of the LES .

• Fig.18 . The Strett a procedure
Source: https://www.stretta -therapy.com/how -stretta -works

• Endoscopic suturing or plication : The Endoscopic Suturing Device (ESD) and the Bard
EndoCinch, invol ves endoscopic suturing .T he NDO Endoscopic Plication System, also
known as the NDO Plicator System, places a full -thickness transmural plication using direct
endoscopic visualization , near the gastroesophageal junction. EsophyX is an endoluminal
therapeutic method that uses a trans -oral and fastener deploying device. The device is passed
into the stomach, where it deploys a series of full -thickness fasteners in order to create a neo
gastro esophageal valve. The EsophyX device creates a transoral incisionless fundoplication
(TIF). Endoscopic plication procedures that are performed through the natural orifice (mouth
or anus ) are examples of natural orifice surgical procedures.

40
• Injection or imp lantation techniques include the following:

o The Plexiglas (polymethylmethacrylate [PMMA]) procedure involves injection of a
polymer material into the submucosa of the proximal lower esophageal sphincter zone in
order to provide bulki ng support to the sphincter and to decrease transient relaxation of
the lowe r esophageal sphincter (T LESRs)
.

o The LINX™ Reflux Management System is an implant that consists of a ring that fits
around the esophagus and is thought to prevent reflux of acid and bile from the stomach
into the esophagus. According to the company website, the LINX system is a flexible
band made of interlinked titanium beads with magnetic cores. The magnetic attraction is
intended to help the (LES) resist opening to gastric p ressures, preventing reflux from the
stomach into the esophagus. A surgeon uses a laparoscopic incision to implant the device
around the patient’s esophagus while the patient is under general anesthesia.

Specific manipulation of the laparoscopic and endos copic devices is a surgical skill requiring
extensive training and experience. Performance of these procedures requires a physician with
experience in the particular endoscopic system in use.

3.8 TREATMENT

Lifestyle advice
Patients should initially be advised on eating healthy and to follow a GERD diet. They should
also be given advice on weight loss if relevant and also on smoking cessation. It can help to eat
often and little, take time to eat meals and avoid eating near bedtime. It is common practice to
advise patients to reduce acidic food (such as citrus fruits), spicy food, alcohol, fizzy drinks,
caffeinated drinks and fatty foods. Following a good acid reflux diet can cure GERD and mean
that patients can reduce t heir need for antacids and medication. Patients are also advised to raise
the head of the bed to help night -time reflux.

41
Drug Treatment
▪ Antacids
They are useful as a first -line treatment and as an OTC (over -the-counter) treatment. Antacids
work predominantly by raising the pH in the esophagus (rather than in the stomach).
▪ Alginate reflux suppressants
Alginate reflux suppressants are forming a protective raft on the surface of the stomach contents.
This barrier suppresses reflux. Th ey can be used on their own for intermittent symptoms, either
on prescription or OTC.
▪ H2 receptor antagonists (H2RAs)
H2RAs, such as ranitidine and cimetidine, work by reducing gastric acid production by parietal
cells. They may suit individual patients but are less effective than PPIs.
▪ Prokinetics
Prokinetics such as metoclopramide and domperidone work by lower esophageal sphincter
pressure, increasing peristalsis, and gastric emptying. They are moderately effective at
treating symptoms of reflux and less effective at healing esophagitis . Prokinetics can be
prescribed on their own but are usually used as an adjuvant to acid suppressing drugs.

• Proton Pump Inhibitors (PPIs)
PPIs reduce acid produ ction in the stomach by inhibiting the proton pump in the parietal cells,
thereby raising the pH (and making the environment less acidic) of the stomach contents. PPIs
are effective at healing esophagitis and at relieving symptoms of acid reflux. PPIs make the
reflux less acidic but do not stop reflux. Proton pump inhibitors should be used at the lowest
effective dose for the shortest period possible and the need for long -term treatment should be
reviewed periodically.

42
IV. SURGERY

4.1 SURGICAL INTERVENTION
Anti-reflux surgery may be used, for example, for patients who do not wish to take long -term
medication or when patients in whom regurgitation ha s not been helped by medication . Doctor’s
guidance suggests that surgery may be an option in patie nts whose quality of life is significan tly
affected by their symptoms.

The surgeon must clearly understand the physiology of the organ he/she is about to change.
Additionally, it is important to obtain baseline postoperative data that may help in the
management of patients when they become symptomatic at a later time.

During the last decade ,surgical intervention for gastroesophageal reflux disease (GERD)
has become increasingly common. Following the introduction of min imally invasive technique s
in 1991, patients became enam ored of this new techniq ue, and referrals from ga stroen terologists
increased substantially. This dramatic increase in the number of operations led to improvements
in this procedure , as surgeons were able to study from a different perspective , the physiology of
the cardia . With better ways to deal with in competent cardia, with new understanding of the
physiology, and with a la rger number of operative proce dures, our knowledge in this area has
also increased.

4.2 SURGICAL TECHNIQUE

Anesthesia and positioning

A single dose of a broad -spectrum antibiotic is given prior to the operation. Al l patients must
receive general anes thesia. Sequential compression devices are placed on each leg to decrease
the risk of deep venous thrombosis, and a Foley catheter is inserted. The patient is placed in a
low lithotomy po sition so that the surgeon can stand between the legs while operating. A

43
beanbag positioned under the patient is used to fashion a seat so the patient may be placed safely
in a steep reverse Trendelenburg position. The assistant stands to the patient’s lef t. The video
monitor is positioned directly over the patient’s head. A self -retaining retractor is secured to the
right side of the bed to hold the liver retractor, avoiding the need for a second assistant.

Pneumoperitoneum and port placement

Pneumoperitoneum i s established through the camera port using a Veress nee dle. A lateral port
site can be used initially if the patient has a midline incision, or an open technique may be used.
We use a Visiport for the first port because it allows observation during entry, thus decreasing
the chance of vascular or bowel injury and significantly increasing the chance of an immediate
diagnosis if such injuries occur. The camera port is placed 10 cm below the costal margin and 2
cm to the left of the midline . Diagnostic lap aroscopy is performed to exclude injury from entry
or other pathology. The uppe r two ports should form an equilateral triangle with the camera port
and are used by the sur geon. This allows the surge on’s instruments to be used at an angle,
enabling correct observation of the tips. The first assistant ports and the liver retractor are placed
at the level of the camera port in the anterior axillary line.

Dissection of the cardia

The left lateral segme nt of the liver is retracted to ex pose the hiatus. We start our dissection by
exposing the left crus (Fig. 19).[66] The surgeon divides the phrenogastric liga ment while the
assistant retracts the fundus infe riorly.The operation starts over the left crus, rather than the more
commonly used right -sided approach because injuries to the struc tures within and posterior to
the gastrohepatic ligament, such as the inferior vena cava and the nerve of Latarjet, are
prevented. This ap proach also makes subsequent di vision of the short gastric vessels easier and
safer.

44

Fig 19. Exposure of left Crus
Source: https://www.ncbi.nlm.nih.gov/pubmed/11814124

Division of the phrenogastric ligament is carried toward the superior pole of the spleen. Along
the superior por tion of the greater curve of the stomach ,the short gastric vessels are divided in
many parts. A ll adhesions of the posterior aspect of the fundus to the splenic vessels, the anterior
aspect of the retroperitoneum , the pancreas, and th e base of the hiatus are divided. This allows
adequate mobilization of the stomach, which has been shown to decrease the incidence of
dysphagia in the postoperative period .[67] Even though clips may be used for division of the short
gastric vessels, it is better to use the Ultrasonic Dissector .These vessels are divided upward to
the previously dissected left crus. The vessels going to the upper pole of the spleen may be very
deep and short , making division dif ficult without prior division of the phrenogastric ligament.

With the left crus completely ex posed and the fundus free ,the left phrenoeso phageal membrane
is incised, en tering the mediastinum betw een the esoph agus and the left crus . The dissection is
continued superiorly and anteriorly, divi ding the peritoneum overlying t he anterior aspect of the
crus.D own the right crus , is extended the line of division , dividing the gastr ohepatic ligament.
For most of the patients, the hepatic branches of the vagus and occasional hepatic branch of the

45
left gastric artery can be preserved with this approach. The inner edge of the right crus is exposed
by dividing the right phrenoesophageal membrane . Once the decussation of the left and right
crus is identified, a pos terior esophageal window is created, taking care to avoid the posterior
vagus nerve. A 0.5-inch Penrose drain is put in this posterior window and secured around the two
vagi and esophagus with a suture or clip.

Esophageal mobilization

Having a Penrose drain around the esophagus allows ef fective retraction during mobilization of
the mediastinal esophagus. M any adhesions to the esophagus can be bluntly divided, with the
vessels and larger adhesions easily divided with the L -shaped electrocautery tip. A lot of c are
must be taken when separating th e pleura from the esophagus. In jury t o the pleura is usually seen
in patients with transmural inflammation from Barrett’s esophagus or esophagitis and in patients
who had previous operations in this area. A small hole in the pleura may be repaired with an
intracorporeal suture, if a pneumothorax does occur. The most impor tant thing is to communicate
with the anesthesiologist when a pleural opening is discovered because a quality monitoring of
airway pressure should be performed. It is prudent in these patien ts to d ecrease the pressure of
the pneu moperitoneum to lessen th e cardiopulmonary effects of in creased intrapleural pressure.
Because carbon dioxide is quickly reabsorbed, pneumot horax in this setting rarely ne cessitates
other intervention.

If the esophag us is difficult to identify, especially in paraesophageal hernias or large hiatal
hernias , a lighted 52F bougie can be inserted. Dissection should not be contin ued with the bougie
in pl ace, so once the surgeon is ori ented, it should be pulled back to the m idesophagus. With
effective retraction and laparoscopic vision, the mediastinal dissection may be carried well into
the mediastinum safely until an adequate length of esophagus (3 cm) is present within the
abdomen and without undue tension.

46
Crural closure

The crura are closed from the junction of the left and right crus, with closure continued
anteriorly. We use 2 -0 silk interrupted sutures placed approximately 0.5 cm apart until the hiatus
is closed well around the esophagus. In the course of tyin g the knot ,it is important to take big
bites of muscle to prevent cut ting the muscle .A 52F bougie advanced across the GE junction at
the end of the closure assures that the hiatus is not closed too tightly. Completely pos terior
closure of very large de fects can angulate the esophagus anteriorly. Then, one or two anteri or
sutures may be placed to com plete the closure. Because of the risk of damaging the esophagus ,
we try to avoid using prosthetic mesh to repair the hiatus. Instead, for de fects that cannot be
closed pri marily, it is prefer ed to make a relaxing incision in the right crus and place mesh over
this defect.[68] A bioprosthesis such as SIS mesh (Surgisis™; Cook Surgical, Blooming -ton, IN)
may be a safer alternative to synthetic material in the hiatus.

Nissen fundoplication

A point on the posterior fundus must be joined with a mirror im age point on the anterior fundus,
in order to create a symmetric fundoplication, . We first place a marking suture on the posterior
fundus 3 cm from the GE junction and 2 cm from the greater curve because it is easy to be come
disoriented when fetching the posterior aspect of the fundus from the rig ht side and under the
esophagus . The previously marked spot on the posterior fundus is held in position without
twisting, and a similar point on the anterior fundus is id entified in front of the esopha gus. Once
the surgeon identifies this point, he/she holds the posterior aspect with the left hand and the
anterior aspect of the stomach with the right hand. We recomme nd at this point, prior to suturing
the fundoplication, that the surgeon pass the left hand, holding the exact place where the suture
will be placed, behind the esophagus without letting go with the right hand (which holds the
anterior aspect of the stomac h). Then , the entire fundopli cation will be held simultaneously and
can be examined in its entirety on the left side of the esophagus. One can then assess the dis tance
of the suture points to its total length and to the greater curvatu re. This step ensures there is no
asymmetry or redundancy to the fundoplication. The points are brought back together, and the
assistant holds the anterior fundus in place while the surgeon places the first suture of the

47
fundoplication. Four sutures 1 cm apart are p laced in or der to create a 3 -cm long fun doplication.
The anterior aspect of the esophagus is not incorporated into the fundoplication sutures. Each
suture is placed while holding the previous suture at the hiatus to ensure that the wrap is created
around the esophagu s and not the stomach. The top of the wrap is then fixed to the esophagus
and hiatus on each side. Another suture is placed from the posterior wrap to the crus, and a final
suture secures the left side of the fundoplication to the diaphragm anteriorly. The se “coronal”
sutures fix the stomach in the abdomen and buttress the hiatal closure to pr event a recurrent
hernia (Fig. 20 ).

Fig.20 Nissen fundoplication
Source: https://www.mayoclinic.org/diseases -conditions/gerd/multimedia/gerd -surgery/img –
20006950

48
4.3 POSTOPERATIVE CARE

When the postoperative nausea subsides ,a clear liquid diet is begun the day of surgery. To
prevent wretching and vomiting, we treat nausea aggressively with dansetron intraoperatively
and postoperatively. Pain is treated with intravenous narcotics the first night via a patient –
controlled analgesia device . The next day, the patient is changed to oral medications in elixir
form. A graduated viscosity diet is advanced slowly over a 4 – to 6-week period. Most patients
may be dischar ged from the hospital within 2 days.

4..4 COMPLICATIONS

GERD is not usually life -threatening.
Still, GERD can result in complications, such as:
• Esophagitis (inflammation of the esophagus)
• Esophageal bleeding, or an ulcer from chronic or severe esophagitis
• Esophageal scarring, which can cause your esophagus to narrow and make swallowing
harder
• Tooth decay
• Sleep apnea
• Respiratory problems, including a cough, hoarseness, wheezing asthma, chronic
laryngitis, chronic bronchitis and pneumonia.
• Barre tt's esophagus (a rare, pre -cancerous condition)
• Esophageal cancer (an even rarer but potentially deadly illness
There are few majo r complications from the Nissen fundoplication . These include esophageal or
gastric perforation and acute postopera tive dysphagia, which may necessitate a second operation

49
for definitive treatment. Death can occur in the cases where people have many severe pulmonary
diseases and can die of respiratory complications. Minor complications rarely have sequelae but
the delay discharge can occur with more frequency. The most common is ileus,which necessitate
placement of a nasogastric tube. Urinary retention occ asionally necessitated catheter ization .
Persistent gas bloat syndrome is controlled with medical therapy and diet modification. In many
of the cases in the first 2 months it can be observed some degree of dysphagia to solids. Knowing
this, it has been developed a diet that emphasizes slow progression toward higher -consistency
foods at the patient’s own pace. Following this regimen, the dysphagia of the patients is not a
significant long -term problem. Longstanding dysphagia is almost always the result of defective
construction of the fundoplication, recurrent hernia , or a torsi on of the esophagus .A
pneumothorax is rare and almost never necessitates a chest tube or other intervention .

4.5 DIFFERENTIAL DIAGNOSIS

The symptoms of acid reflux and GERD can be mimicked by other medical conditions
(extraesophageal and esophageal diseases) such as gastroparesis, Zenker diverticulum,
achalasia, peptic ulcer disease, gallstones, functional dyspepsia, and angina pectoris. These
conditions can be diagnosed by their failure to respond to aggressive antisecretory therapy with a
PPI and by the use of othe r diagnostic tests such as endoscopy, esophageal manometry,
ultrasound, barium esophagram, nuclear emptying studies, and various cardiac tests. Although
GERD is the most common cause of esophagitis there are other causes such as tablet or pill
injury, infec tions, or radiation esophagitis. These need to be considered in cases that are difficult
to manage and in those who have a problem with their immune system or who are older. If you
have persisting symptoms of heartburn then you should consult your physicia n or family doctor.

50
4.6 PREVENTION
We can prevent future episode of GERD h eartburn by avoiding any triggering factors like:
Foods To Avoid
For some people, avoiding some or all of these potential dietary triggers may be helpful in
preventing future episodes of GERD and relieving symptoms:
1.Alcohol
2.Caffeine (chocolate, coffee, soda, tea)
3.Citrus fruits & juices
4.High -fat foods, including fried foods & full -fat dairy products
5.Mint (peppermint, spearmint)
6.Onions & peppers
7.Spicy foods
8.Tomato products

Lifestyle Tips
• For many people, these tips can be helpful in relieving symptoms & preventing future
episodes of GERD:
• Spend time walking after a meal to aid digestion
• Avoid large meals; eat small frequent meals throughout the day
• Avoid use of tobacco products
• Sleep with your head elevated
• Avoid lying down at least 2 hours after eating a meal
• Exercise regularly
• Maintain a healthy weight, as excess weight contributes to reflux

51

SPECIAL PART

52
5.1 INTRODUCTION

Over the past years th ere have been many studies and l iterature about different types of
minimal invasive repair procedures all over the world. In this particular study I will be
exclusively looking into the repair surger y done in our modern day times which is laparoscopic
surgical technique.
The study took place in Bucharest, Romania at the Floreasca Emergency Hospital in the
department of general surgery and was done by looking through the medical files of patients
from January 1st 2014 till 30thJune 2018 .
I have done a retrospective study on 65 cases of patients over the interval of 4 years who
had the diagnostic of GERD and who had to choose between taking medic ation or undergoing
the Nissen f undoplication .

5.2 AIM OF STUDY

The aim of this research is to identify the surgical technique as a treatment st rategy in the
management of the gastroesophageal reflux for the patients who are presenting to the hospital in
early and late stages.
This research will have the cases distributed by gender,age,home regio n,BMI,diagnostic
tests,comorbidity,admission reason,laboratory findings,postoperative stay and quality of life
after the laparoscopic surgery Nissen fundoplication .As the patients can also take medication for
the gastroesophageal reflux,this thesis will compare between the two of them(laparascopic
surgery and taking medication) to see which of the two used methods is the most beneficial for
the patient and in what ways each of them surpasses the other.

Main o bjectives :
▪ To check if sex is a major factor
▪ To find out if age is a major factor

53
▪ To find out if obesity is a major factor
▪ To see which of the two types of procedures is most frequently laparoscopic surgery or
taking medication .
▪ To check if comorbidity can affect the surgery.
▪ To asses the hospital stay.

The data was collected from the hospital archived files which fit the criteria of the
retrospective study being done and which had the information required for this study. The
information about the patients were r egistered at the time of the first presentation,during the
hospital stay and after the surgery.

Materials and Methods :
▪ Clinical presentation sheets
▪ Surgical protocols
▪ Microsoft Excel and SPSS

5.3 PATIENT SELECTION

The patients were selected after clinical and positive diagnosis of GERD . Patients
presenting to the hospital usually complaint about heartburn, regur gitation and epigastric pain .
These symptoms are usually aggravated in time by people having tabacco pr oducts,citrus fruits
and juices,high -fat foods,eating large meals, spicy food,people laying down immediately after
eating a meal . The appearance of these signs and symptoms are closely monitored due to the fact
that these symptoms are well known to progre ss over periods of time. For each study that was
done certain parameters were taken into consideration and recorded :

▪ Patients Data : Name, weight, height, age, gender ,home region
▪ Etiopathogenic data : Co morbidities, incidence, past medical history
▪ Clinical diagnostic tests: endoscopy,radiography,abdominal ultrasonography,
24-hour ph -monitoring ,barium esophagram,manometry
▪ Laboratory investigation: General biological investigations

54
5.4 INCLUSION CRITERIA OF THE STUDY
• The informal consent being signed by the patient .
• Minimum age for inclusion in the study was 18 years old .
• All the investigations were performed since the suspicion of the disease must be
well documented.
• All lab oratory findings must be well documented from the patients’ admission to
discharge, in order to follow patients’ progress.
• Gender of the patients was also vital from the study as GERD is considered to
have many implications with sex.
• Type of treatment – medica l treatment or surgery treatment .
• Pre and post operatory stay analysis

5.5 EXCLUSION CRITERIA OF THE STUDY
• People younger than 18 and older than 80 years old
• People having radioth erapy for another disease when p resenting to the
hospital.They will be reevaluated after finishing the radiotherapy sessions.
• Patients having multiple trauma.
• Biological laboratory findings that cannot allow the patient to have anesthesia or
any type of surgical intervention.
• Epilepsy and psychiatric disorders.

55
5.6 OBSERVATIONAL RESULTS

❖ GENDER

Table II

Figure 21 .A Pie chart representing gender distribution.
Gender Number
M 35
F 30
F
46%
M
54%Patients by gender
F
M

56
Observation:

As deduced from table II , the data gave unshakable evidence supporting all the
most recent literature that GERD occur mostly in males. The research shows that 54%
of the subjects were males and 46% of them were females as made clearly in figure21.

Explanation:

There is no clear association of gender or age with GERD symptoms, but ¤male gender
¤advancing age and ¤white race are associated with a high risk of GERD complications.
There are many reports that suggest an association between GERD symptoms and gender but the
reports are different: some of them say that the prevalence is greater in men , some say that it is
greater in women ,while others find no difference by gender . Knowing that males are always
working hard and having a lot of physical effort and exercise, professional body builders who
have weight lifting are more predisposed to get GERD.

❖ AGE

Table III Age interval Number
21 to 30 5
31 to 40 15
41 to 50 20
51 to 60 15
61 to 70 0
71 to 80 10

57
51520
15
010
NUMBERDistribution by age groups
21 to 30 31 to 40 41 to 50 51 to 60 61 to 70 71 to 80

Fig.22.Distribution by age groups

Observation:

In the above table III and figure 22, we can see various age distributions that have
been obtained from our study. It clearly shows a very high peak point according to age
at which our patients had GERD .The ages 41 -50 years experienced the m ost cases of
GERD. Another observation to be noted is that in the intervals of ages 31 to 40 and 51
to 60 the occurrence rate was approximately the same. The f inal observation seen in
table III and figure 22 is that people are starting to have signs and s ymptoms of GERD
even if they are actually young.

Explanation:

A viable explanation for this phenomenon of why a majority of cases appeared in
the older generations would be the weakening of the organs because of advancing age.
As for the young and act ive individuals, most of them were reported as having
epigastric pain debuting after strenuous work or physical exercise, these activities
contributing to GERD. Another important thing to keep in mind for the young and some

58
middle age classes is that some individuals might have other pathologies that can
contribute to GERD:hiatal hernia, Zollinger -Ellison syndrome ,obesity, high blood
calcium levels.

❖ HOME REGION

Total= 65
F M
Rural 13 4
Urban 16 31
Table IV

Figure 23 Distribution by home region
1613
314
0 5 10 15 20 25 30 35URBANRURALHome region
M F

59

Fig. 24. Home region in percentage

Observation:
Talking about the home region , table IV and fig. 23 are explaining that the highest pick point is
seen at the males that live in the urban area. This means that the most people who had Nissen
fundoplication came from the urban areas.Also,from the fig.24 it can be seen that even though
the percentage of pe ople from rural areas is lower than the perc entage from the urban areas ,
there are still people that ar e counting on surgeons and coming to undergo the laparoscopic
surgery .

Explanation:
When it comes to the home region, we must compare the fact that people from the urban areas
are having more medical education, they are getting more information about different
pathologies and they are getting earlier to the doctor, in comparison to the ones from the rural
areas. Also the st ress met in different jobs, can highly provoke GERD and all the complications.
The risk is for the males that are working hard eating high fat foods and drinking a lot of
alcohol.
73%27%Home region
Urban
Rural

60

❖ COMORBIDITY

Females Males
With comorbidities 23 29
Without comorbidities 7 6
Table V

Fig.25 Distribution by comorbidity
237
296
0 5 10 15 20 25 30 35WITH COMORBIDITIESWITHOUT COMORBIDITIESComorbidity
Males Females

61

Fig. 26 Percentage of comorbidity

Observation:
From table V and fig. 25 , it can easily be seen that most of the patients, both males and females
suffered from a lot of comorbidities,such as(table VI ): cardiovascular pathologies,
bronchopulmonary pathologies,congenital pathologies,enlarged prostate,gast rointestinal
pathologies, BMI>25.From fig.26 it can be seen that only 20% of the patients were without
comorbidity.The o nes without comorbidity were the perfect type of patients that can undergo the
Nissen Fundoplication.

Explanation
There are a lot of comorbidities that can appear with age. The cases of the patients who have
comorbidities, are discussed by the surgeons whether they can undergo or not the surgery. The
ideal situation for the surgery is not having any other comorbidity associated.Everything was
taken into consideration before taking the deci sion to operate. The most frequent comorbidities
are the cardiovascular pathologies like : high blood pressure, arrhythmias, coronary artery
diseases and myocardial infarction in their past history. The second most frequent are the GI and 80%20%Comorbidity
With Without

62
bronchopulmonary pathologies that are found relatively in the same number of patients and it is
due to reasons like having a C OPD, asthma and bronchiectasis.

Table VI

❖ BMI

Table VII NUMBER OF PATIENTS
Cardiovascular pathologies 42
Bronchopulmonary pathologies 39
Gastrointestinal pathologies 33
Congenital pathologies 2
Enlarged prostate 9
BMI >25 25
BMI Number of cases
<25(Normal weight) 15
25-30(overweight) 24
30-35(moderately obese) 25
35-40(severely obese) 1

63

Fig.27. Distribution by BMI

Observation
The BMI(body mass index) is ratio between an individual's height and weight which is then
corresponded with their age to determine what type of physical status they have. From table VII
and fig.27 we are able to see that the majority of patients(38 %) were moderately obese and 37%
of them were being overweight.Only one patient that presented to the hospital was severely
obese. Talking about a normal BMI ratio, only 23% of the patients had normal weight.

Explanation:
BMI is used as a screening tool to indicate whether a person is overweight ,underweight,
obese or having a healthy weight for their height.If a person's BMI is out of the healthy BMI
range, their health risks may significantly increase. In this study we n oticed that the majority
(38%%) of patients were the ones that were moderately obese while the lowest percentile was
only one patient with a severely obese score . This leads us to understand that there is a direct
connection between being overweight and having GERD in most of the cases.
<25, 15, 23%
25-30, 24, 37%
30-35, 25, 38%
35-40, 1, 2%BMI

64

❖ LABORATORY FINDINGS

Laboratory findings Number of patients
Without modifications 41
With modifications 24
Table VIII

Fig 28 Laboratory findings

63%37%LABORATORY FINDINGS
Without modifications
Without modifications

65
Observation
From table VIII and fig. 28 it can easily be seen the fact that there are not so many patients 37%
who had their laboratory findings modified. Also there are 63% patients that had no modification
in their lab findings. The laboratory tests were : blood count,ALT,AST, bi lirubin, cholesterol,
creatinin,GGT,glucose,potas sium,sodium,triglycerides,urea, INR, APTT.

Explanation
Even though there were so many patients that had their laboratory tests normal,we must not fall
into the idea that they literally had nothing that can change their health. Actually the unmodified
laboratory tests may appeared due to the fact that the patients were still on medication for their
pathologies or some of them had no comorbidity.

❖ CLINICAL DIAGNOSTIC TESTS

Number of patients Percent value
endoscopy
31 47,69%
radiography 63 96,92%
abdominal ultrasonography 65 100%
Table IX

66

Fig 29. Clinical diagnostic tests
Observation
Table IX and fig. 29 are explaining the clinical diagnostic tests that were done for the patients
with GERD. All of them 100% had the abdominal ultrasonography . 96,92% of the patients
accepted to have the radiography, and 2 of them refused the investigation. The endoscopy was
not so popular , only 47,69% of the patients accepted it.

Explanation
The reason why many of our patients chose the abdominal ultrasonography was because it is a
non-invasive method of diagnose and it does not have a bad impact on the health of the
patient.The patients that did not agree to have the radiography stated that they were afraid of the
radiation exposure.Knowing the risks of the endoscopy,few of the patients agreed with the
investigation,most of them did not accept it bec ause of its complications.

YESNO
010203040506070
endoscopy radiography abdominal
ultrasonography31636534
2
0Clinical diagnostic tests
YES NO

67
❖ ADMISSION REASON

Fig.30 Distribution by admission reason

Number of
patients Percent Value
Heartburn 40 61,53%
Regurgitation 31 47,69
Dysphagia 9 13,84%
Chest pain 15 23,07%
Epigastric pain 27 41,53%
Vomiting 5 7,69%
Chronic cough 11 16,92%
Sleep disturbance 23 35,38%
Table X 31
40
9
15
27
5
11
23ADMISSION REASON
Number of patients

68

Observation
Fig. 30 and table X are explaining the reasons why patients are presenting to the hospital. Most
of them had heartburn as a symptom 61,53 %. At a similar percentage, were regurgitation with
47,69% and epigastric pain with 41,53%. Few patients had vomiting 7,69% and dysphagia
13,84% as an admission reason.

Explanation
Most of the s ymptoms that appeared were with or without esophageal injury .The main symptom
of GERD is heartburn. Heartburn is discomfort felt behind the breastbone as a burning sensation.
It tends to get worse if the person lies down or bends over and also after eating food.However,
not all people with GERD experience heartburn, and there are other possible symptoms:nausea
or vomiting, chest pain angina like,epigastric pain, respiratory and laryngeal symptoms: chronic
cough, hoarseness, asthma worsening, sleep disturbances.

❖ MEDICATION VS. NISSEN FUNDOPLICATION

Number of patients Percentage
Medication 36 55%
Nissen Fundoplication 29 45%
Table XI

69

Fig.31. Medication vs. Nissen fundoplication

Observation
From Figure 31 and table XI , it can be seen that the number of patients that chose medication
over laparoscopic Nissen fundoplication is wide bigger 36 over 29 . Talking about 6 5 patients,
the percentage is 55% for the ones choosing medication .

Explanation
As we just saw, the medication for GERD is the most used method for the patients I took
for this study and it is almost the same in most of the literature from around the world. The
55%
45%Number of patients
Medication
Nissen Fundoplication

70
reason for this could have many factors like people having a shorter perio d of time for staying in
the hospital ,as well as medication being a more affordable method. For certain aspects like
infection or talking about surgery itself ,some of the patients consider getting a Nissen
fundoplication to be life threatening. Also ,sometime a very important aspect is the financial
situation and the surgeon’s availability. There are also cases when a surgery cannot be performed
due to the comorbidities of the patients. Anti-reflux surgery may be used, for example, for
patients in wh om regurgitation has not been helped by any medication , or when patients do not
wish to take a long-term medication. People in our study had two reasons:
1. Their life quality was significantly affected by their symptoms
2. They do not wish for a long -term treatment

❖ HOSPITAL STAY

HOSPITAL STAY after Nissen fundoplication Number of patients
1-3 days 21
4-6 days 5
6-8 days 1
>8 days 2
Table XII

Fig.32 The hospital stay for the patients who had Nissen fundoplication
1-3 DAYS 4-6 DAYS 6-8 DAYS >8 DAYS 72,41%
17,24%
3,44% 6,89%Hospital stay
Number of patients

71
Observation
About the hospital stay, table XII and fig.32 are explaining the number of patients that had
Nissen fundoplication and how many days did they spend in the hospital after the surgery .The
information about the patients were registered at the time of the first presentation,duri ng the
hospital stay and after the surgery. Dividing the days of stay, it can be seen that most of them
spent from 1 to 3 days in the hospital 72,41% . The stay at the hospital is decreasing with days
from 17,24% to 3 ,44%. Also, there is an exception; there were 2 patients that spent more than 8
days in the hospital.

Explanation
Being a minimal invasive technique of solving GERD, the laparoscopic procedure doesn’t need
many days of recovery. This being said, here comes the explanation of the decreasin g number of
days that the patients stayed in the hospital. About the exception, that 2 of the patients spent
more than 8 days in the hospital, this was due to the fact that they had much comorbidity that
affected the period of recovery. Seeing this and the minimum of days spent in the hospital, it
could easily be understood that people who are presenting to the hospital just to take a
prescription for medication, they could easily spend that day just to have the procedure -Nissen
fundoplication and as a resu lt they would have no more a long term treatment for the future.

❖ QUALITY OF LIFE

Medication Nissen
Fundoplication
Better quality
of life 7 19,44% 26 89,6%
Lower quality
of life 29 80,55% 3 10,34%
Table XIII

72

Fig 33. The quality of life after a period of time
Observation
Seeing table XIII and figure 33, in case of our all 65 patients, it can be seen that the patients who
chose Nissen f undoplication had a major improve on their life quality 89,6%.On the other hand,
the ones that preferred medication over surgery, 80,55% of them had a lower quality of life.
There were also 10,34% of th e patients who got the Nissen fundoplication and that did not feel
any changes in the quality of life.

Explanation
The reason why some of the patients who chose medication over surgery had no changes in their
life quality is because they had to take a long -term treatment that sometimes can be very
disappointing and time -consuming. The patients that chose Nissen fundoplication had the highest
rate in changing their life quality. With the result of the surgery, from that moment, the patients
will not need any medication for GERD as a long -term treatment.
MedicationNissen fundoplication
051015202530
Better quality of life Lower quality of life72926
3Quality of life
Medication Nissen fundoplication

73
5.7 RESULT SUMMARY

❖ Based on our study of gastro esophageal reflux, a male has a greater incidence to have GERD
while females have low risk of getting gastro esophageal reflux .
❖ Second observation is the effect of GERD on age, relying in our statistics results that the
patients between 41 to 50 years old are more prone to getting GERD and this generates the
treatment approach not so difficult. Elder patients are with increased comorbidities, data
result s displayed a high number in cardiovascular pathology and bronchopulmonary d isease.
❖ According to the results of our research most of the patients came from the urban areas, and
most of them were males.
❖ Moreover, clinical complains that we have registered were different compared among the
patients but still some symptoms were with high frequency, for instance
heartburn,regurgitati on, epigastric pain.
❖ Another observation was about the laboratory tests ,many patients had their tests normal but
this was due to the fact that the patients were still on medication for their pathologies or
some of them had no comorbidity.
❖ We were able to see that the majority of patients were moderately obese and almost the same
number of patients were being overweight.Only one patient that presented to the hospital
was severely obese. Talking about a nor mal BMI ratio, only 23% of the patients had normal
weight.
❖ Doing the clinical diagnostic tests, all the patients chose to have the abdominal
ultrasonograpy.From a total of 65 patients, 2 of them did not agr ee to have the radiography
and almost half of the patients did not agree to have the endoscopy,being afraid of the
complications.
❖ Based on our research, the medica l treatment is the most used method for patients with
GERD.
❖ Being a minimal invasive method of solving GERD, the laparoscopic procedure does no t
need many days of recovery and most of the patients spent only 1 to 3 days in the hospital.
Additionally, our research has demonstrated a high number of patients that had a better
quality of life after choosing to undergo the Nissen fundoplication.

74
CONCLUSION

❖ After doing this research paper on comparison between the two main treatment types for
GERD , I have found some solid undisputable facts as well as some surprises. My main goal
was to compare between them and to see which is the one that is mor e superior to the other.

❖ After looking through the files of different patients , I saw that sex is a risk factor, the
majority of patients who had GERD were males .

❖ In this study, the distribution by age helped us to see that surprisingly the age is not a major
factor. We would have expected to see the highest number of elder patients to have
GERD,but the ones that were suffering from it were the middle aged ones.
❖ After doing the BMI ratio for the patients presenting to the hospital,we saw that there is a
direct connection between being overweight and having GERD in most of the cases. Having
the patients with higher BMI range s, their health r isks may significantly increase and then
obesity should be considered a major factor.

❖ I also noticed that the patients preferred taking medication over having the Nissen
fundoplication and this is almost the same in most of the literature from around the world.
The main reason for this is that the medication represents a more affordable method than the
laparoscopic surgery. Also , some the patients that did not do the Nissen fundoplication were
the ones suffering from many comorbidities that did not allow them to undergo the surgery.

❖ My final conclusion after doing this thesis paper is that both methods : laparoscopic surgery
and taking medication have almost the same efficiency for the gastroesophageal reflux , but
the one that changed the most the quality of life was the Nissen fundoplication .

75
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