hiatal hernia

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Transcript hiatal hernia

 Hiatus
hernia is a herniation
of viscera,
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Most commonly the
stomach,
Into the mediastinum
through the esophageal
hiatus of the diaphragm
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Four types of hiatus hernia are distinguished
with:
type I, or sliding hiatal hernia comprising at
least 95% of the overall total
A sliding hiatal hernia is one in which the
gastroesophageal junction and gastric cardia
slide upward as a result of weakening of the
phrenoesophageal ligament attaching the
gastroesophageal junction to the diaphragm
at the hiatus.
The main significance of sliding hernias is the
propensity of affected individuals to have
GERD.
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II, III, and IV hiatal
hernias
 are all subtypes of
paraesophageal hernia in
which the herniation into the
mediastinum includes a
visceral structure other than
the gastric cardia.
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A lower esophageal mucosal ring, also called
a B ring, is a thin membranous narrowing at
the squamocolumnar mucosal junction
Its origin is unknown but B rings are
demonstrable in about 15% of people and are
usually asymptomatic.
When the lumen diameter is less than 13
mm, distal rings are usually associated with
episodic solid food dysphagia and are called
Schatzki rings.
Patients typically present older than 40
years, consistent with an acquired rather than
congenital origin.
 One
of the most common
causes of intermittent food
impaction,
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also known as "steakhouse
syndrome" as meat is a typical
instigator.
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Web-like constrictions higher in the esophagus
can be of congenital or inflammatory origin.
Asymptomatic cervical esophageal webs are
demonstrated in about 10% of people and
typically originate along the anterior aspect of
the esophagus.
When circumferential, they can cause
intermittent dysphagia to solids similar to
Schatzki rings and are similarly treated with
dilatation.
The combination of symptomatic proximal
esophageal webs and iron-deficiency anemia in
middle-aged women constitutes PlummerVinson syndrome .
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Esophageal diverticula are categorized by
location with the most common being :
epiphrenic,
hypopharyngeal (Zenker's),
mid esophageal.
Epiphrenic and Zenker's diverticula are false
diverticula involving herniation of the mucosa
and submucosa through the muscular layer of
the esophagus.
These lesions result from increased
intraluminal pressure associated with distal
obstruction.
 Mid-esophageal
and epiphrenic
diverticula are usually
asymptomatic until they enlarge
sufficiently to retain food and
cause dysphagia and
regurgitation.
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Esophageal motility disorders are
diseases attributable to esophageal
neuromuscular dysfunction
commonly associated with dysphagia,
chest pain, or heartburn.
The major entities are achalasia,
diffuse esophageal spasm (DES), and
GERD.
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Achalasia is a rare disease caused by loss of
ganglion cells within the esophageal myenteric
plexus
with a population incidence of about 1:100,000
usually presenting between age 25 and 60.
Functionally, inhibitory neurons mediate
deglutitive lower esophageal sphincter (LES)
relaxation and the sequential propagation of
peristalsis.
Their absence leads to impaired deglutitive LES
relaxation and absent peristalsis.
Increasing evidence suggests that the ultimate
cause of ganglion cell degeneration in achalasia
is an autoimmune process
 Clinical
manifestations may
include dysphagia, regurgitation,
chest pain, and weight loss.
 Patients
with advanced achalasia
are at risk for bronchitis,
pneumonia, or lung abscess from
chronic regurgitation and
aspiration.
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Achalasia is diagnosed by barium swallow x-ray
and/or esophageal manometry;
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endoscopy has a relatively minor role other than to
exclude pseudoachalasia.
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The barium swallow x-ray appearance is of a dilated
esophagus with poor emptying, an air-fluid level, and
tapering at the LES giving it a beak-like appearance
The diagnostic criteria for achalasia with esophageal
manometry are impaired LES relaxation and absent
peristalsis.
Because manometry identifies early disease before
esophageal dilatation and food retention, it is the
most sensitive diagnostic test.
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Therapy is directed at reducing LES
pressure so that gravity and esophageal
pressurization promote esophageal emptying
LES pressure can be reduced by pharmacologicals
therapy, forceful dilatation, or surgical myotomy
Pharmacologicals therapies are relatively
ineffective but are often used as temporizing
therapies.
Nitrates or calcium channel blockers
Botulinum toxin, injected into the LES under
endoscopic guidance, inhibits acetylcholine
release from nerve endings and improves
dysphagia in about 66% of cases for at least 6
months.
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only durable
therapies for achalasia
are:
 pneumatic dilatation
and
 Heller myotomy.
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DES is manifested by episodes of
dysphagia and chest pain attributable
to abnormal esophageal contractions
with normal deglutitive LES relaxation.
Radiographically, DES has been
characterized by tertiary contractions
or a "corkscrew esophagus“
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Esophageal chest pain closely mimics
angina pectoris.
Features suggesting esophageal pain
include pain that is nonexertional,
prolonged, interrupts sleep, is mealrelated, is relieved with antacids, and
is accompanied by heartburn,
dysphagia, or regurgitation
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Although the defining criteria are currently
disputed, DES is diagnosed by manometry.
Endoscopy is useful to identify alternative
structural and inflammatory lesions that may
cause chest pain.
The only controlled trial showing efficacy was
with an anxiolytic.
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current conception of GERD is
to encompass a family of
conditions with the commonality
that they are caused by the :
 gastroesophageal
reflux resulting
in either troublesome symptoms
or an array of potential
esophageal and extraesophageal
manifestations.
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The best defined subset of GERD patients,
albeit a minority overall, have esophagitis.
Esophagitis occurs when refluxed gastric
acid and pepsin cause necrosis of the
esophageal mucosa causing erosions and
ulcers.
esophagitis results from excessive reflux,
often accompanied by impaired clearance of
the refluxed
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Three dominant mechanisms of esophagogastric
junction incompetence are recognized:
(1) transient LES relaxations
(2) LES hypotension
(3) anatomic distortion of the esophagogastric
junction inclusive of hiatus hernia.
Transient LES relaxations account for at least 90%
of reflux in normal subjects or GERD patients
without hiatus hernia
Factors tending to exacerbate reflux regardless
of mechanism are :
abdominal obesity, pregnancy, gastric
hypersecretory states, delayed gastric emptying,
disruption of esophageal peristalsis, and
gluttony.
Inherent
in the
pathophysiologic
model of GERD is that
gastric juice is harmful
to the esophageal
epithelium.
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Heartburn and regurgitation are the typical
symptoms of GERD.
Somewhat less common are dysphagia and chest
pain.
In each case, multiple potential mechanisms for
symptom genesis operate that extend beyond the
basic concepts of mucosal erosion and activation
of afferent sensory nerves.
Specifically, hypersensitivity and functional pain
are increasingly recognized as confounding
factors.
Nonetheless the dominant clinical strategy
is of empirical treatment with acid
inhibitors, reserving further evaluation for
those who fail to respond.
 With
chest pain, cardiac disease
must be carefully considered.
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the case of persistent
dysphagia, chronic reflux can lead
to the development of a peptic
stricture or adenocarcinoma, each
of which benefits from early
detection and/or specific therapy.
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Extraesophageal syndromes with an
established association to GERD include:
chronic cough, laryngitis, asthma, and dental
erosions.
Potential mechanisms for extraesophageal
GERD manifestations are of either
regurgitation with direct contact between the
refluxate and supraesophageal structures or
via a vagovagal reflex wherein reflux
activation of esophageal afferent nerves
triggers efferent vagal reflexes such as
bronchospasm, cough, or arrhythmias.
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infectious, pill, or eosinophilic esophagitis, peptic
ulcer disease, dyspepsia, biliary colic, coronary artery
disease, and esophageal motility disorders.
It is especially important that coronary artery disease
be given early consideration
The distinction among etiologies of esophagitis is
usually easily made by endoscopy with mucosal
biopsies
The ulcerations seen in peptic esophagitis are usually
solitary and distal, whereas infectious ulcerations are
punctate and diffuse.
Eosinophilic esophagitis characteristically exhibits
multiple esophageal rings, linear furrows, or white
punctate exudate.
Esophageal ulcerations from pill esophagitis are
usually singular and deep at points of luminal
narrowing, especially near the carina
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The complications of GERD are related to :
chronic esophagitis (bleeding and stricture)
and the relationship between GERD and
esophageal adenocarcinoma.
Barrett's metaplasia, endoscopically
recognized by tongues of reddish mucosa
extending proximally from the
gastroesophagealjunction or
histopathologically by the finding of
specialized columnar metaplasia, is
associated with at least a 20-fold increased
risk for development of esophageal
adenocarcinoma.
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Lifestyle modifications are routinely
advocated as GERD therapy.
(1) avoidance of foods that reduce lower
esophageal sphincter pressure, making them
"refluxogenic" (these commonly include fatty
foods, alcohol, spearmint, peppermint,
tomato-based foods, possibly coffee and
tea);
(2) avoidance of acidic foods that are
inherently irritating; and
(3) adoption of behaviors to minimize reflux
and/or heartburn.
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The dominant pharmacologic approach to
GERD management is with inhibitors of
gastric acid secretion
reducing the acidity of gastric juice does not
prevent reflux, but it ameliorates reflux
symptoms and allows esophagitis to heal.
Proton pump inhibitors (PPls) are more
efficacious than histamine, receptor
antagonists (HzRAs), and both are
superior to placebo.
 Laparoscopic
Nissen
fundoplication,
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wherein the proximal stomach is
wrapped around the distal esophagus
to create an anti reflux barrier, is a
surgical alternative to the
management of chronic GERD
Grade A
Grade B
Grade
C
Grade D
 Incidence
rates for adenocarcinoma of the
esophagus have been increasing in several
Western countries
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In contrast, rates for SCC have been steadily
decreasing in these same countries
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Familial aggregation of esophageal cancer has
been described in regions with a high incidence
of esophageal (SCC), such as China.
Familial aggregation of Barrett's esophagus has
also been described.
Whether this represents common environmental
risk factors or inherited predisposition is
unknown.
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the extent to which hereditary factors are
involved in the pathogenesis of esophageal
cancer remains uncertain.
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major risk factors for SCC of the
esophagus in the United States are smoking
and alcohol consumption
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major risk factors for SCC in the
“esophageal cancer belt” of Iran and Asia are
not well understood, but are thought to
include poor nutritional status, low intake of
fruits and vegetables, and drinking beverages
at high temperatures
 Lower
socioeconomic status
 Smoking
and alcohol : In the United States,
Western Europe
 Underlying
esophageal disease
achalasia,ingestion of lye during childhood
 Tylosis:
a rare disease associated with
hyperkeratosis of the palms of the hands and
soles of the feet
 Bisphosphonates
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The major risk factors for adenocarcinoma of
the esophagus are:
Barrett's esophagus
 gastroesophageal reflux disease
Smoking
high body mass index
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Gastroesophageal reflux disease
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Most, if not all, esophageal adenocarcinoma arises
from a region of Barrett's metaplasia
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more than 50 percent of cases of adenocarcinoma
have no history of symptomatic reflux disease
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Among patients who have Barrett’s esophagus, the risk
of developing esophageal cancer is increased at least
30-fold above that of the general population, but the
absolute risk of developing cancer in patients with
Barrett's metaplasia is low (estimated annual cancer
incidence 0.12 percent in one population-based
Danish study)
 SCC:
located in the midportion
 Adenocarcinoma:
the majority of cases are
located near the GE junction
and are associated with
Barrett's esophagus
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progressive solid food dysphagia often
accompanied by weight loss.
This usually occurs once the esophageal
lumen diameter is less than 13 mm
Chronic gastrointestinal blood loss from
esophageal cancer is common
Tracheobronchial fistulas are a late
complication
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Early esophageal cancers appear
endoscopically as superficial
plaques, nodules, or ulcerations
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lesions appear as
strictures, ulcerated masses ,
circumferential masses or large
ulcerations
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staging usually begins with a CT scan of the
chest and upper abdomen (limited value for
locoregional tumor staging)
Patients without evidence of metastatic disease
by CT undergo endoscopic ultrasonography
(EUS)
 T1Tumor
invades lamina propria, muscularis
mucosae, or submucosa
T1a:Tumor invades lamina propria or muscularis
mucosae
T1b:Tumor invades submucosa
 T2:Tumor
invades muscularis propria
 T3:Tumor invades adventitia
 T4:Tumor invades adjacent structures
T4a:Resectable tumor invading pleura, pericardium, or
diaphragm
T4b:Unresectable tumor invading other adjacent
structures, such as aorta, vertebral body, trachea, etc.
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N Classification
N0 – no regional lymph node metastasis.
N1 – 1 to 2 positive regional lymph nodes.
N2 – 3 to 6 positive regional lymph nodes.
N3 – greater than or equal to 7 positive
regional lymph nodes
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M Classification
M0 – no distant metastases.
M1 – distant metastases
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The prognosis for patients with esophageal
carcinoma is poor.
Fewer than 5% of patients survive 5 years after
the diagnosis;
thus, management focuses on symptom control.
Surgical resection of all gross tumor (i.e., total
resection) is feasible in only 45% of cases
About 20% of patients who survive a total
resection live 5 years.
The efficacy of primary radiation therapy (55006000 cGy) for squamous cell carcinomas is
similar to that of radical surgery
 Combination
chemotherapy and
radiation therapy as the initial
therapeutic approach, either alone
or followed by an attempt at
operative resection, seems to be
beneficial.
 When administered along with
radiation therapy, chemotherapy
produces a better survival
outcome than radiation therapy
alone.