esophageal diseases 1

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Post graduate courseEsophageal diseases

• Prof Dr Yasser M Fouad
  Prof Dr Hanaa K Fathelbab
• Dr Reem Y Mousa
  Dr Hamdy Sayed
• Dr Rofida K Moftah

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Dr Rofida
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Anatomy of Oesophagus
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It is fibro-muscular tube 12 cm in child 25 cm
in adults extends from the lower border of the
cricoid cartilage (C6) to the cardiac orifice
of the stomach T11
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PARTS OF OESOPHAGUS

• The esophagus has been subdivided into 3
  portions, as follows
• -The cervical portion extends from the
  cricopharyngeus to the suprasternal notch
• -The thoracic portion extends from the
  suprasternal notch to the diaphragm
• -The abdominal portion extends from the diaphragm
  to the cardiac portion of the stomach.

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Applied anatomy

• -venous drainage
• cervical part inferior thyroid vein
• thoracic part azygos hemiazygos veins
• Abdominal part drain into left gastric
  vein
• Varices

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Applied anatomy

• Lymphatic Drainage
• -cervical part cervical LNs
• -Thoracic part Mediastinal LNs
• -Abdominal part Coeliac LNS
• CARCINOMA

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Arterial supply

• The cervical portion
• the inferior thyroid artery
• The thoracic portion
• bronchial and esophageal branches of the
  thoracic aorta
• The abdominal portion
• ascending branches of the left phrenic and left
  gastric arteries

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Oesphageal constrications

• -from incisor teeth
• -15 cm UOS
• -25 cm Aortic arch
• -27 cm Lt main bronchus
• -40 cm opening in diaphragm
• F.B impaction

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Esophageal Sphincters

• -UPPER -LOWER
• -Which Anatomical ??
• Upper Esophageal Sphincters

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Lower Esophageal Sphincter

• It is physiological by many factors
• -intra abdominal pressure
• -pincock action of diaphragm
• -Angle of Hiss
• -plug mucosal rosette of stomach

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Dr Hamdy
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HISTOLOGY OF THE ESOPHAGUS
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• Mucosa
• Epithelium
• non-keratinized stratified squamous epithelium
  basal zone has basophilic proliferative cells
  with minimal cytoplasm, usually 3-4 cells thick,
  cells then flatten and mature as they approach
  lumen / surface.
• Lamina propria
• fibrovascular connective tissue between
  epithelium and muscularis mucosa folds into
  slender papillae that projects into epithelium,
  usually less than 2/3 of epithelial thickness
  may contain gastric cardia-like mucus
  particularly in distal esophagus.
• Muscularis mucosa
• smooth muscle bundles oriented longitudinally
  begins at cricoid cartilage and becomes thickened
  distally.
• (Z-line is the squamocolumnar junction which is
  histologically irregular. The lower esophageal
  sphincter is located in this area.)

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• Submucosa
• Loose connective tissue with vessels,
  lymphatics, occasional white blood cells,
  lymphoid follicles (rare), Meissners plexus
  (sparse ganglia) and nerves, submucosal glands
  lined by mucinous cells that produce acid mucin
  and bicarbonate.
• Muscularis propria
• Inner circular and outer longitudinal layers
  proximally includes skeletal muscle from
  cricopharyngeus and inferior pharyngeal
  constrictor muscles. It contains Auerbach
  (myenteric) plexus.
• Note longitudinal muscle originates as two bands
  from cricoid cartilage that incompletely digitate
  and leaves a bare V-shaped region (area of
  Laimer) that exposes the underlying circular
  muscle and creates area of weakness where
  Zenkers diverticulum may occur.
• Adventitia
• loose connective tissue (not consistent serosa),
  so tumors and infections spread readily.

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Dr Reem
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Physiology of esophegus

• The only function of the esophegus is to
  transport food bolus from the pharynx to the
  stomach where the process of digestion begins
• Efficient transport by the esophagus requires a
  coordinated, sequential motility pattern that
  propels food from above and clears acid and bile
  reflux from below , this movement is known as
  peristalsis.

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• Peristalsis is a sequential, coordinated
  contraction wave that travels the entire length
  of the esophagus, propelling intraluminal
  contents distally to the stomach. The LES relaxes
  during swallows and stays opened until the
  peristaltic wave travels through the LES, then
  contracts and redevelops resting basal tone.

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• Primary peristalsis is the peristaltic wave
  triggered by the swallowing center and travels at
  a speed of 2 cm/s responsible for pushing the
  food bolus
• The secondary peristaltic wave is induced by
  esophageal distension from the retained bolus,
  refluxed material, or swallowed air. The primary
  role is to clear the esophagus of retained food
  or any gastroesophageal refluxate.
• Tertiary contractions are simultaneous, isolated,
  dysfunctional contractions. These contractions
  are nonperistaltic, have no known physiologic
  role, and are observed with increased frequency
  in elderly people. Radiographic description of
  this phenomenon has been called presbyesophagus.

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Neuromuscular coordination

• Striated muscle regions
• The motor innervation to the striated muscle
  regions of the esophagus is somatic arising from
  the nucleus ambigus of the brain stem vagus
  nerve to give excitatory fibers only to striated
  muscle fibers through release of acetyl choline

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• Smooth muscle portion has a more complicated
  innervation
• - extrinsic ( located outside the wall of
  esophegus)
• 1-parasympathetic preganglionic fibers arise from
  dorsal motor nucleus vagus nerverelay in
  myenteric plexus through release of acetyl
  choline to activate nicotinic receptors of
  myenteric plexus ( exicitatory fibers mediate
  contraction)
• 2-sympathetic postganglionic fibers arise from
  cervical ,thoracic and celiac ganglia vagus and
  peri vascular nerves myenteric and submucosal
  plexus inhibition of nitric oxide release
  through activation of muscarinic receptors(
  inhibitory fibers mediating relaxation)

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• -intrinsic ( located inside the wall of
  esophegus)
• 1)myenteric plexus located between the circular
  and longitudinal layers of muscles
• 2)sub mucosal plexus (in sub mucosa)
• Each plexus form a network that terminates at the
  muscle fibers controlling its action
• Another type of bipolar cells (interstitial cells
  of Kajal) is present between the nerve fibers and
  muscles seems to play a role in neurotransmission

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Dr Yasser
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Oesophagus classification by aetiology

• Congenital atresia, stenosis, fistulas, webs
• Infection fungal infection, viral infection,
  Chagas disease
• Physical/Trauma lacerations
• Chemical/Toxic gastro-oesophageal reflux disease
  (GORD)
• Circulatory disturbances oeophageal varices
• Immunological disturbance eosinophilic
  oesophagitis
• Degenerative disorders
• Iatrogenic pill oesophagitis
• Idiopathic achalasia
• Various radiation, psychosomatic
• Pre-neoplastic/ Neoplastic Barretts oesophagus
  -gt adenocarcinoma squamous cell carcinoma

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DR Rofida
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CASE 1

• A 2-year-old boy presented to a local hospital
  after ingesting an unknown amount of hair and
  grease remover.
• The patient's past medical and surgical history
  were unremarkable.
• The patient underwent intubation at the outside
  emergency department because of respiratory
  distress and was transferred to our facility.
• He had obvious burns to the lips and mouth,
  though not severe.
• Doctor took decision of Endoscopy

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-The Timing of endoscopy ??

• - Which type of endoscopy ??

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The Timing of endoscopy ??

• -are recommending earlier endoscopy and
  suggesting a wait of only 12 hours and a total
  wait of no more than 24 hours after ingestion for
  early assessment and treatment.
• -Endoscopy past 48 hours is discouraged because
  of progressive wall weakening and increased risk
  of perforation
• - Most agree that strong alkali ingestion
  mandates endoscopy, while asymptomatic or
  questionable ingestions may be observed,
  according to some sources

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The Timing of endoscopy ??

• FIRST 48 hours from ingestion corrosive
• pass 48 hours!!! ?
• After 14 up to 21 days from ingestion corrosive

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Which type of endoscopy ??

• -flexible esophagoscopy,
• is the most effective method for visualizing the
  extent of esophageal injury
• provides important information about the stomach
  and duodenum
• - Rigid esophagoscopy
• may be used but should not be extended beyond
  the site of caustic burn because of an increased
  risk of perforation.
• is recommended for nasogastric tube placement and
  airway management.

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• The patient received flexible endoscopy within
  the 24 hours following injury.
• He was found to have erythema and small
  ulcerations in both the esophagus and stomach.
  His injuries were deemed grade 2a.

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Endoscopic grading system

• Grade 0 Normal
• Grade 1 Mucosal edema and hyperemia
• 2 ULCER
• Grade 2A Superficial ulcers, bleeding, exudates
• gt Excellent prognosis
• Grade 2B Deep focal or circumferential ulcers
• 3 NECROSIS
• Grade 3A Focal necrosis
• gt Develop strictures 70-100
• Grade 3B Extensive necrosis
• gt Early mortality rate 65

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Endoscopic grading system
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• The patient was given multiple broad spectrum
  antibiotics without steroids
• Analgesia to control pain
• . He had repeated endoscopy on day 14

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DR Yasser
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Corrosive ingestions
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• Common alkaline-containing sources
• Ammonia-containing products
• Oven-cleaning products
• Swimming pool cleaning products
• Automatic dishwasher detergent
• Hair relaxers
• Clinitest tablets
• Cement

• Common acid-containing sources
• Toilet bowl cleaning products
• Automotive battery liquid
• Rust-removal products
• Metal-cleaning products
• Cement-cleaning products
• Drain-cleaning products

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• Symptoms
• Dyspnea , Dysphagia, Oral pain and
  odynophagia
• Chest pain , Abdominal pain, Nausea and
  vomiting
• life-threatening hypocalcemia following ingestion
  of hydrogen fluoride (in some rust removers).
• Material Safety Data Sheets (MSDS), online
  databases, and consultations with the local
  poison center are all ways for a clinician to
  rapidly familiarize themselves with unfamiliar
  caustics agents.

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• Physical Examination
• Stridor
• Hoarseness
• Dysphonia or aphonia
• Respiratory distress, tachypnea, hyperpnea
• Cough Tachycardia
• Oropharyngeal burns
• Subcutaneous air
• Acute peritonitis - Abdominal guarding, rebound
  tenderness, and diminished bowel sounds
• Hematemesis

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• Indications of severe injury include the
  following
• Altered mental status
• Peritoneal signs
• Evidence of viscous perforation
• Stridor
• Hypotension
• Shock

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• Laboratory studies may include the following
• pH testing of product and saliva A pH less than
  2 or greater than 12.5 indicates greater
  potential for severe tissue damage
• Complete blood count (CBC) and electrolyte, blood
  urea nitrogen (BUN), creatinine, and ABG levels
  may all be helpful as baseline values and as
  indications of systemic toxicity
• Liver function tests and a disseminated
  intravascular coagulation (DIC)
• Urinalysis and urine output may help guide fluid
  replacement
• Serum calcium level and cardiac monitoring and
  serial ECGs may be needed

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Upright chest radiograph in all cases of
caustic ingestion. Findings may include
pneumomediastinum or other findings suggestive of
mediastinitis, pleural effusions,
pneumoperitoneum, aspiration pneumonitis, or a
button battery (metallic foreign body). If
contrast studies are obtained, water-soluble
contrast agents are recommended because they are
less irritating to the tissues in cases of
perforation. Computed tomography (CT) scans will
often be able to delineate small amounts of
extraluminal air, not seen on plain radiographs.
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Endoscopy Because of the risk of increased
injury, esophagoscopy should not be performed in
patients with evidence of esophageal or
gastrointestinal perforation, significant airway
edema, or necrosis and in those who are
hemodynamically unstable. Obtaining meaningful
information from endoscopy after treatment with
activated charcoal is very difficult. Routine use
of activated charcoal is not recommended in
caustic ingestions.
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Obtain MSDS sheets when possible for workplace
exposures. The product container or labels may be
available. Avoid exposure to health care
workers. Do not induce emesis or attempt to
neutralize the substance by using a weak acid or
base. Small amounts of a diluent may be
beneficial if administered as soon as possible
after a solid or granular alkaline ingestion, to
remove any particles that are adhering to the
oral or esophageal mucosa.
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Water or milk may be administered in small
amounts. It is very unlikely to be of any benefit
after more than 30 minutes. This practice is
controversial Some of the literature available
on this topic discourages the use of diluents
because of the concern of inducing emesis
resulting in re-exposure of tissue to caustic
agent. Diluents should not be used with any acid
ingestion or liquid alkaline ingestion. The risk
of vomiting with re-exposure of the oral or
esophageal mucosa to the offending substance can
result in worsening injury or perforation.
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Airway control Because of the risk of rapidly
developing airway edema, the patients airway and
mental status should be immediately assessed and
continually monitored. Equipment for endotracheal
intubation and cricothyrotomy should be readily
available. Gentle orotracheal intubation or
fiberoptic-assisted intubation is preferred.
Blind nasotracheal intubation should be avoided
due to the increased risk of soft-tissue
perforation. If a difficult airway is
anticipated, IV ketamine can be used to provide
enough sedation to obtain a direct look at the
airway. Cricothyrotomy or percutaneous needle
cricothyrotomy may be necessary in the presence
of extreme tissue friability or significant edema.
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Gastric emptying and decontamination Gastric
lavage by traditional methods using large-bore
orogastric Ewald tubes are contraindicated in
both acidic and alkaline ingestions because of
risk of esophageal perforation and tracheal
aspiration of stomach contents. Esophageal
perforation is rare. NGT suction may be of
particular value following ingestion of zinc
chloride, mercuric chloride, or hydrogen
fluoride, unless signs of perforation are
present. This should be done after consulting
with a regional poison control center. Activated
charcoal is relatively contraindicated in caustic
ingestions because of poor adsorption and
endoscopic interference.
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Dilution Dilution may be beneficial for ingestion
of solid or granular alkaline material if
performed within 30 minutes after ingestion using
small volumes of water. Because of the risk of
emesis, carefully consider the risks versus
benefits of dilution. Do not dilute acids with
water this would result in excessive heat
production. Neutralization Do not administer a
weak acid in alkaline ingestions or a weak
alkaline agent in acid ingestions. There is a
risk of heat production resulting from this
exothermic reaction. In addition, the risk of
emesis makes this a hazardous intervention.
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• Obtain a surgical consultation when the following
  are expected or observed
• Perforation
• Mediastinitis
• Peritonitis

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• Antibiotic, Cephalosporin (Third Generation)
• Antibiotic, Penicillin and Beta-lactamase
  Inhibitor
• Proton Pump Inhibitor
• Analgesic, Narcotic

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• Further Outpatient Care
• Psychiatric evaluation for all patients with
  intentional ingestion
• Follow-up esophagram 3-4 weeks postingestion
• Patients who develop esophageal stricture as a
  result of caustic ingestion can be treated with
  esophageal balloon dilatation (EBD). In
  children, dilatation should be performed gently
  with balloons of gradually increasing appropriate
  diameters over consecutive sessions. EBD
  treatment was significantly faster and shorter in
  patients who began EBD earlier (mean, 15 days)
  after caustic ingestion than in those who began
  it later (mean, 34 days).

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DR Hamdy
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A 32-year-old man presents to the ED 90 minutes
after an acute episode of vomiting, which caused
him to have severe chest pain. The patient has an
odor of alcohol on his breath. His friends state
that the patient was "okay" before the vomiting
episode. His blood pressure is 95/50 mm Hg.
Electrocardiography (ECG) is performed and shows
sinus tachycardia at 130 beats per minute without
any ST-segment changes. His oral temperature is
99.9F he has an oxygen saturation of 98 on
room air.
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His chest radiograph is shown. What is the most
likely diagnosis?1- Acute myocardial
infarction2- Esophageal perforation (Boerhaave
syndrome)3- Left-sided empyema4- Perforated
gastric ulcer
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His chest radiograph is shown. What is the most
likely diagnosis?1- Acute myocardial
infarction2- Esophageal perforation (Boerhaave
syndrome)3- Left-sided empyema4- Perforated
gastric ulcer
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 Chest computed tomography (CT) studies usually
confirm the diagnosis of Boehaave syndrome they
may also demonstrate a false tract originating
from the esophagus (arrow).
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Boerhaave first described the spontaneous rupture
of the esophagus in 1724. It typically occurs
after forceful emesis.
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Pathophysiology Esophageal rupture in Boerhaave
syndrome is postulated to be the result of a
sudden rise in intraluminal esophageal pressure
produced during vomiting, as a result of
neuromuscular incoordination causing failure of
the cricopharyngeus muscle to relax. The syndrome
commonly is associated with overindulgence in
food and/or alcohol
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The classic clinical presentation of Boerhaave
syndrome usually consists of repeated episodes of
retching and vomiting, typically in a middle-aged
man with recent excessive dietary and alcohol
intake. These repeated episodes of retching and
vomiting are followed by a sudden onset of severe
chest pain in the lower thorax and the upper
abdomen. The pain may radiate to the back or to
the left shoulder. Swallowing often aggravates
the pain. Typically, hematemesis is not seen
after esophageal rupture, which helps distinguish
it from the more common Mallory-Weiss tear. .
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• Signs
• Subcutaneous emphysema is particularly helpful
  in confirming the diagnosis
• tachypnea and abdominal rigidity.
• Tachycardia, diaphoresis, fever, and hypotension
  are common
• Unusual findings may include the following
• Peripheral cyanosis
• Hoarseness of voice due to recurrent laryngeal
  nerve involvement
• Tracheal and mediastinal shift
• Proptosis
• Later stages of illness may manifest with signs
  of infection and sepsis. Symptoms may include
  fever, hemodynamic instability, and progressive
  obtundation. Establishing a diagnosis in the
  later stages can be quite difficult because
  septic complications begin to dominate the
  clinical picture. Early diagnosis is critical.

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Laboratory Studies Patients may present with
leukocytosis and a left shift. Many patients
present with a pleural effusion. Thoracentesis
with examination of the pleural fluid can aid in
diagnosis. Undigested food particles and gastric
juices usually are found. If no gross particles
are found, cytology can confirm or exclude their
presence, but time is of the essence. The pH of
the pleural fluid will be less than 6, and the
amylase content will be elevated.
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Upright chest radiography This is useful in the
initial diagnosis because 90 of patients reveal
an abnormal finding after perforation. The most
common finding is a unilateral effusion, usually
on the left. This corresponds with the fact that
most perforations occur in the left posterior
aspect of the esophagus. Other findings may
include pneumothorax, hydropneumothorax,
pneumomediastinum, subcutaneous emphysema, or
mediastinal widening. Overall, 10 of chest
radiographs are normal. This can be at least
partly explained by the delayed radiographic
development of mediastinal and subcutaneous
emphysema. These findings may take an hour or
more after perforation to appear on the chest
radiograph
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Esophagraphy Esophagraphy helps to confirm the
diagnosis. It typically shows extravasation of
contrast into the pleural cavity. An esophagram
outlines the length of the perforation and its
location, which aids in the decision on whether
to use a thoracic or abdominal surgical
approach. Initially, use a water-soluble
contrast, such as Gastrografin. It has 90
sensitivity. It may have false-negative results
in up to 20 of patients. The use of barium in
patients affected with Boerhaave syndrome has
been associated with severe mediastinitis. CT
scanning CT scanning can reveal decisive criteria
for diagnosis, it is helpful in patients too ill
to tolerate esophagrams, and it localizes
collections of fluid for surgical drainage. It
can also demonstrate periesophageal air tracks
that are suggestive of perforation, although it
may not precisely localize the site of
perforation. Visualization of adjacent structures
is possible, which expands the differential
diagnosis in patients with chest pain and vomiting
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Endoscopy is not commonly used to aid in
diagnosis of Boerhaave syndrome. It carries the
additional risks of increasing the size and
extent of the original perforation and forcing
additional air through the perforation into the
mediastinum or pleural cavity.
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• Ideal management for Boerhaave syndrome involves
  a combination of both conservative and surgical
  interventions.
• Intravenous volume resuscitation
• Administration of broad-spectrum antibiotics
• Prompt surgical intervention
• The decision to use a conservative (medical
  intervention only) or an aggressive (medical plus
  surgical intervention) approach depends on the
  following factors
• Time delay in presentation and diagnosis
• Extent of perforation
• Overall medical condition of the patient
• Surgical intervention is the standard of care in
  most cases

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• Conservative management consists of the
  following
• Intravenous fluids should be instituted.
• Antibiotics Imipenem/cilastatin (Primaxin)
  offers good broad-spectrum coverage.
• Nasogastric suction should be applied.
• Keep the patient NPO.
• Adequate drainage with tube thoracostomy.
• Early use of nutritional supplementation
  Evidence suggests that for hastening recovery, a
  jejunostomy tube feeding may be favored over
  hyperalimentation

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Traumatic rupture

• 1- Boerhaave syndrome
• 2- Mallory Weiss tear

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Overview of Mallory-Weiss Syndrome Mallory-Weiss
syndrome is characterized by upper
gastrointestinal bleeding secondary to
longitudinal mucosal lacerations (known as
Mallory-Weiss tears) at the gastroesophageal
junction or gastric cardia. The original
description by Mallory and Weiss in 1929 involved
patients with persistent retching and vomiting
following an alcoholic binge.  However,
Mallory-Weiss syndrome may occur after any event
that provokes a sudden rise in the intragastric
pressure or gastric prolapse into the esophagus,
including antecedent transesophageal
echocardiography
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Risk Factors for Mallory-Weiss Tears vomiting,
straining, hiccupping, coughing, blunt abdominal
trauma, and cardiopulmonary resuscitation.
Hiatal hernia is a predisposing factor and is
found in 35-100 of patients with Mallory-Weiss
tears Iatrogenic tears are uncommon,
considering the frequency with which patients
retch during endoscopy.
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Evaluation of Mallory-Weiss Tears Hematemesis is
present in 85 of patients. In fact, the classic
presentation consists of an episode of
hematemesis following a bout of retching or
vomiting Less common presenting symptoms
include melena, hematochezia, syncope, and
abdominal pain and aspirin use has been reported
in up to 30 of patients Specific physical
signs are generally not present for Mallory-Weiss
tears. However, physical findings relate to the
rate and the degree of gastrointestinal blood
loss. Tachycardia, hypotension, orthostatic
changes, or overt shock may be evident
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Endoscopy Endoscopic diagnosis of a Mallory-Weiss
tear is readily made by identifying active
bleeding, an adherent clot, or a fibrin crust
over a mucosal split within or near the
gastroesophageal junction. On average, the split
is 2-3 cm in length and a few millimeters in
width. Most patients (gt80) present with a single
tear. The usual location of the tear is just
below the gastroesophageal junction on the lesser
curvature of the stomach (between 2 and 6 o'clock)
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Initial management Monitor the patients vital
signs, obtain serial hemoglobin and hematocrit
values (q6h initially), watch for clinical signs
of rebleeding, correct coagulopathy if possible,
and maintain hemodynamic support with fluid and
blood replacement. Control or eliminate
precipitating factors, such as nausea and
vomiting. Acid suppression (eg, omeprazole) and
antiemetic drug therapy (eg, prochlorperazine)
are sufficient in most patients presenting with a
Mallory-Weiss tear. Transfuse, generally, for
hemoglobin levels less than 8 g/dL (lt 10 g/dL for
patients with cardiopulmonary disease). Five to
35 of patients require some form of
intervention, mostly endoscopic Dietary
constraints Fasting is restricted to
hemodynamically unstable patients and to those
who require repeat endoscopic intervention within
a short time because of uncertainty regarding the
effectiveness of endoscopic therapy or possible
complication of the initial therapy. Unless
nausea or vomiting is an issue, patients can
resume oral intake following endoscopy, starting
with a clear- or full-liquid diet and advancing
as tolerated to a regular diet within 48 hours.
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Contact thermal treatment A contact thermal
modality, such as multipolar electrocoagulation
(MPEC) or heater probe, with or without
epinephrine injection, is typically used to treat
an actively bleeding Mallory-Weiss tear.
Epinephrine injection Epinephrine injection
(110,000-120,000 dilution) reduces or stops
bleeding via a mechanism of vasoconstriction and
tamponade. This treatment is usually combined
with a more definitive therapy (eg, thermal
therapy). 0.5-1 mL are injected around and into
the bleeding point. Epinephrine injection is best
avoided in patients with active cardiovascular
disease. Sclerosant injection Successful use of
sclerosants, such as alcohol or polidocanol, has
been reported. Safer alternatives exist, and
sclerosant injection is not recommended by some
authors because of its potent tissue-damaging
effects, risk of deep tissue necrosis, and
potential for perforation.
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Argon plasma coagulation Reports on the use of
the argon plasma coagulator (APC) in the
treatment of bleeding Mallory-Weiss tears are
limited, but this noncontact device is gaining in
popularity owing to its ease of use. Band
ligation Endoscopic band ligation has been shown
to be effective for treating bleeding
Mallory-Weiss tears.  Band ligation should be
particularly useful for bleeding Mallory-Weiss
tears associated with portal hypertension and
gastroesophageal varices, in which thermal
therapy is not recommended. Hemoclip
placement Endoscopic hemoclip placement using the
2-pronged clip devices is also effective for
Mallory-Weiss tears. The margins of the tear may
be approximated, starting at the distal end of
the tear and applying successive clips in a
cephalad fashion. Alternatively, only the
bleeding point can be targeted for hemoclip
placement Angiotherapy with either selective
vasopressin infusion or embolization of the left
gastric artery can be performed in patients whose
lesions have failed to respond to endoscopic
therapy or who are at high risk of endoscopic
complications. .
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Surgical Management Surgical oversewing of the
tear is reserved for the occasional bleeding case
that is refractory to endoscopic therapy or
angiotherapy
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DR Reem
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Refresh your endoscopic memory
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Guess .. What could it be
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Herpes simplex esophagitis
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• Odynophagia and dysphagia usually in
  immunocompromised patient
• Endoscopy revealed numerous vesicles that
  ulcerate to form small (2 cm), shallow volcano
  shaped ulcers
• microscopic exam of mucosal brushings shows
  intranuclear eosinophilic inclusions
• Treatment acyclovir 400mg orall or 200 mg IV /8
  hours for 2 weeks
• Or valacyclovir,famciclovir or foscarnet

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And this?
89
CMV esophagitis
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• Odynophagia (common) and dysphagia (less common)
  usually in immunocompromised patient
• Larger (2cm), oblong, with a sharply demarcated,
  "punched-out" appearance, and a bland base.
• On biopsy, CMV basophilic intranuclear inclusions
  in epithelial cells and fibroblasts of the
  densely inflamed granulation tissue of the ulcer
  base.
• Treatment IV ganciclovir 5mg/kg for 24 weeks
• Or foscarnet

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This one?

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Monilial (candida) esophagitis (cottage cheese
esophegus )
93

• As other types of esophagitis it is common in
  immunocompromised individuals
• White- yellow plaques that may be confluent in
  longitudinal manner ,may be associated with
  necrotic or ulceration.
• Biopsies show candida pseudo hyphae
• Treatment
• In non AIDS patient oral nystatin or
  clotrimazole
• In AIDS patient IV fluconazole

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HIV idiopathic ulcer
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HIV esophagitis

• HIV as a state of immune compromision is
  associated with different types of esophagitis
• Candida esophagitis in (50-79)
• CMV esophagitis (10-40) , overlapped candida and
  CMV esophagitis occurs in nearly 20
• Herpetic esophagitis (lt5)
• Malignant esophageal ulcers as in Kaposi sarcoma
• Idiopathic HIV ulcers ( dramatic response to
  corticosteroid therapy)

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Tuberculous esophagitis

• Rare condition occurs by one of 5 routes
• (1)swallowing infected sputum in the presence of
  an antecedent esophageal disease
• (2)direct extension from adjacent structures, for
  example, mediastinal lymph nodes
• (3)extension of tuberculous involvement of the
  pharynx or larynx.
• (4)back flow in lymphatics draining the
  esophagus.
• (5)hematogenous spread from a distant site

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Pill induced esophagitis

• Occurs in patients taking medications improperly
  esp. elderly ( while supine or with too little
  water)
• Commonly on top of pre existing condition as
  motor disorder or diverticulum
• Pills get attached to esophageal mucosa causing
  necrosis and ulceration through local contact
  with caustic ingredients

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Pill induced esophagitis
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Treatmnt

• Discontinuation of offending drug
• Sucralfate 1gm/6 hours for 24 weeks
• Cocktail equal parts of ( lidocaine antacid
  diphenhydramine)
• Once daily PPI prevents aggravation by reflux
• Advise your patient to take pill with full glass
  of water while in upright position

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Corrosive esophagitis

• Occurs as result of accidental ingestion of
  caustic substance in children or suicidal
  ingestion in adult
• Most common ingestants are wash cleaner ( sodium
  hydroxide), Bleach ( sodium hypochlorite) or
  detergents ( sodium tri poly phosohates)
• Risk of acute ulceration and perforation followed
  by stricture formation

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• Urgent esophagoscopy in first 48 hours could be
  done after exclusion of perforation by swallow
  using gastrograffin
• Cautious endoscope not extending beyond area of
  severe damage to avoid perforation
• Emergency esophagectomy or esophagogastrectomy to
  avoid fatal mediastinitis
• In absence of these complications supportive
  management in the form of IV fluids and
  antibiotics
• Low dose of steroids are given without proven
  efficacy

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Radiation esophagitis

• Usually occurs after chest radiation
• Severe inflammation and ulceration followed by
  hemorrhage , perforation and fistula formation
• Typical retrosternal pain, dysphagia and
  odynophagia
• Barrium swallow and endoscopy demostrates the
  extent of the disease
• Endoscopic biopsy exclude infectious cause
• Liquid diet and IV fluids together with the same
  prescription mentioned in pill induced
  esophagitis
• Stricture may need dilatation or even
  esophagectomy with jejunal or ileal interposition

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Eosinophilic esophagitis

• Eosinophilic esophagitis is a clinicopathologic
  disease characterized by
• Symptoms of food impaction and dyphagia in
  adults, and feedingintolerance or GERD in
  children.
• More than 15 eosinophils/high power field on
  pathologic examination.
• Exclusion of other disorders with similar
  clinical or pathologic findings,especially GERD.

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Epidemiology

• For unclear reasons, there seems to be an
  increasing incidence of eosinophilic esophagitis
  that is not solely accounted for by increasing
  recognition.
• Disease occurs in all age groups but symptoms
  usually appear either in early childhood,
  adolescence, or before the fourth decade of life.
• Males comprise 70 of cases.

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Pathophysiology

• The pathogenesis of eosinophilic esophagitis is
  unknown.
• There is some thought that the disease process
  originates from an immune-mediated response to a
  swallowed allergen.
• Once eosinophils have infiltrated the esophageal
  mucosa, their presence appears to trigger a
  self-sustaining cascade of inflammatory mediators.

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Risk factors

• There seems to be an increased incidence of
  eosinophilic esophagitis in pediatric patients
  with a history of asthma, allergic rhinitis,
  eczema, and food or environmental allergies. This
  association has not been fully studied in the
  adult population.
• There is also a reported association of
  eosinophilic esophagitis in adults with
  eosinophilic gastroenteritis and peripheral
  eosinophilia.

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Diagnosis

• History and clinical picture
• Lab
• A CBC can be performed to evaluate for
  peripheral eosinophilia, although this phenomenon
  is more frequently seen in the pediatric
• Imaging
• A barium swallow may add further data regarding
  a patients anatomy and assessing for dominant
  strictures, but is not required in the routine
• management of this disease.

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Diagnostic Procedures

• EGD with biopsies along the length of the
  esophagus should be performed to confirm the
  diagnosis of eosinophilic esophagitis.
• Gross mucosal abnormalities include longitudinal
  furrowing, friability, edema, longitudinal
  shearing, whitish exudates, , narrow caliber
  esophagus, rings, and transient or fixed rings.
• The esophageal mucosa is grossly abnormal by
  endoscopy in more than half of patients.

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• Biopsy specimens should be obtained regardless
  of the gross appearance of the esophageal mucosa.
  Biopsies should be obtained in the stomach and
  duodenum to determine whether the disease is
  confined to the esophagus or is a manifestation
  of another process, such as eosinophilic
  gastroenteritis or inflammatory bowel disease.
• Patients will have normal pH monitoring of the
  distal esophagus in contrast to GERD.
• Some physicians have suggested allergen skin
  testing in order to avoid potential precipitating
  foods or allergens.

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Treatment

• Medications
• Medications are the mainstay of treatment for
  eosinophilic esophagitis.
• First Line
• Currently, the most commonly accepted course of
  treatment is topical corticosteroids.
• Second Line
• Systemic corticosteroids have been shown to have
  significant benefit in pediatric patients.

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• Third Line
• A humanized antiIL-5 antibody, mepolizumab, has
  been studied over the past few years and
  preliminary results show that it is effective in
  improving the clinical and pathologic disease in
  patients with eosinophilic esophagitis.

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Non reflux esophagitis
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Describe the pattern of esophageal contractions
in the following disorders

• 1- D E S
• 2- Achalasia
• 3- Nutcraker esophagus
• 4- I E M
• 5- Scleroderma

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Achalasia
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