GIT DR.

LAPUZ SECTION A

DEVELOPMENTAL ANOMALIES
DISEASES OF THE ESOPHAGUS  Relatively common
 50% have other anomalies : Vertebral, Anal, Cardiac, Tracheal,
Two major functions of the esophagus
Esophageal, Renal, Limb system (VACTERL)
1. Transport of food bolus from the mouth to the stomach
2. Prevention of retrograde flow of gastrointestinal content  Esophageal atresia and tracheoesophageal fistula are the most
Anatomy common developmental anomalies
 18-26 cm long hollow  Other diseases: esophageal stenosis, duplications, vascular anomalies,
muscular tube esophageal rings and webs
 Esophageal wall consist of
mucosa, submucosa,
Developmental stages
muscularis propia and
 4th week- develops tracheo-
adventitia
bronchial diverticulum and
 No serosa
subsequently separates to become
the primitive respiratory tract
Mucosal layer
 7-8th week - the luminal epithelium
•Lined by nonkeratinized,
proliferates and almost completely
stratified squamous
occludes the foregut with only residual
epithelium
channels persisting
•Z -line (ora serrata);
Squamocolumnar junction  10th week – recanalize
- demarcation between the
lighter esophageal mucosa and
the redder
gastric mucosa(columnar ESOPHAGEAL ATRESIA AND TRANSESOPHAGEAL FISTULA
epithelium)

Muscular layer
•Upper 1/3 - - skeletal muscle
•Middle 1/3 - mixed
•Lower 1/3 - smooth muscle

Levels of Narrowing
1. Upper esophageal sphincter
2. Aortic arch Most common
3. Left mainstem bronchus
4. Diaphragm
5. Lower esophageal
Sphincter

Upper esophageal sphincter (skeletal

muscle)
 Consists of :
 Inferior pharyngeal
constrictor muscles, and
 Cricopharyngeus
 both are innervated by Esophageal atresia (A) and Tracheoesophageal fistulas (B through E) are
excitatory somatic lower the most common developmental anomalies of the esophagus.
motor neurons. In the most common tracheoesophageal fistula, the trachea communicates
 CN 5, 7, 12 with the distal segment of the atretic esophagus (B).
The next most common type is the H-type tracheoesophageal fistula, in which
Lower esophageal sphincter the trachea communicates with an otherwise normal esophagus (C).
(thickened smooth muscle) Tracheoesophageal fistulas in which the trachea communicates with both upper
 Innervated by parallel sets of and lower segments of an atretic esophagus (D)
parasympathetic excitatory and
inhibitory pathways Atresia
 Supported by skeletal muscle of  failure of the primitive foregut to recanalize
the diaphragmatic crura, which  isolated atresia is rare
surrounds the LES and acts as  upper esophagus ends in a blind pouch and the lower esophagus connects
an external LES to the stomach
 suspected prenatally by the development of polyhydramnios and at birth by
SYMPTOMS OF ESOPHAGEAL regurgitation of saliva and gasless abdomen
DISEASE  rapid onset of choking, coughing, regurgitation of first feeding
1. Dysphagia - sensation of Fistula
“sticking” or obstruction of the o tract between 2 epithelium- lined organs or vessels that normally do not
passage of food through the connect
mouth, pharynx or esophagus o failure of the lung bud to separate completely from the foregut atresia and
2. Odynophagia - painful fistula
swallowing
3. Globus sensation - sensation
of lump lodged in the throat
that is felt irrespective of
swallowing that occurs in the
setting of anxiety or obsessive-
compulsive disorders
4. Heart burn/pyrosis - burning
retrosternal discomfort that arises from the epigastrium and may
radiated toward the neck. Most common esophageal symptom
VASCULAR ANOMALIES
5. Regurgitation - effortless appearance of gastric or esophageal content
Dysphagia Lusoria
in the mouth
o esophagus is compressed by an aberrant right subclavian artery arising from
6. Chest pain – excessive salivation resulting from the vagal reflex the descending aorta and passing behind the esophagus
triggered by acidification of the esophageal mucosa o The right subclavian artery in this circumstance arises from the left side of
Usually experienced as a pressure type sensation in the mid chest, the aortic arch and courses from the lower left to the upper right side posterior
radiating to the mid back, arms, or jaws. Similar to cardiac pain to the esophagus

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 confirms or established the diagnosis

 combination of aperistalsis and incomplete relaxation of LES after
swallowing typifies Achalasia
Endoscopy
 for ruling out secondary causes of Achalasia particularly gastric carcinoma
TREATMENT
Medical:
 Nitrates - isosorbide dinitrate (2.5-5 sublingually or per orem) before meal
 Ca channel blocker - Nifedipine (20-30mg SL) before meal
 Sildenafil
Endoscopic:
 Botolinium toxin injection - block the cholinergic excitatory nerves in
sphincter
- effective in 60% for 6 months
HETEROTROPHIC GASTRIC MUCOSA  Balloon dilatation/Bougienage
o also known as esophageal inlet patch, is a focus of gastric type - effective in 85% of patients
epithelium in the proximal cervical esophagus - repeated technique
o the estimated prevalence is 4.5%  Per orem Esophageal Myomotomy (POEM)- advantage of surgical
o Inlet patch is thought to result from incomplete replacement of disruption of diaphragmatic hiatus and more rapid recovery
embryonic columnar epithelium with squamous epithelium
o Majority of patches are asymptomatic, but acid production can occur as
most contain fundic type of gastric epithelium with parietal cells
ESOPHAGEAL WEBS
o Congenital or inflammatory in origin
o Characterized by one or more thin horizontal membranes of stratified
squamous epithelium
o Located within the upper (common) and midesophagus (rare)
o Rarely encircle the lumen completely (protrudes from the anterior wall,
extending laterally but not posteriorly)
o Asymptomatic hypopharyngeal webs are demonstrated in 10% of normal
individuals
o Primary symptom is dysphagia
o Hypopharyngeal webs + iron-deficiency anemia + dysphagia = PLUMMER-
VINSON or PATTERSON KELLY SYNDROME
o Risk factor : Squamous cell carcinoma of the esophagus
o Best demonstrated on an esophagogram, lateral view
o Treatment is by bougienage/dilatation ESOPHAGEAL DILATATION using a pneumatic balloon
MOTILITY DISORDERS (Bougienage)
ACHALASIA
o Definition :“ does not relax”
o Rare disorder
o loss of ganglion cells within the myenteric (Auerbach’s) plexus
o Such damage can potentially affect excitatory ganglion neurons (cholinergic),
inhibitory ganglion neurons (NO ±VIP), or both
o These neurons mediate deglutitive inhibition (including LES relaxation) and
the sequenced propagation of esophageal peristalsis; their absence offers a
unifying hypothesis for the key physiologic abnormalities of achalasia;
Pathophysiology
o Loss of intramural inhibitory neurons while the direct excitatory effect remains
unopposed muscle remains contracted
o Long standing achalasia leads to enervation leads to dilatation and sigmoid
deformity of the esophagus with hypertrophy of LES
o APERISTALSIS and FAILURE of LES to RELAX
SURGICAL
Differential diagnosis:
o Carcinoma (Tumor) that infiltrates the esophagus (commonly from the  Heller’s extra mucosal myotomy of LES (circular muscle is incised)
gastric fundus or distal esophaguas, “pseudoachalasia”  Laparoscopic myotomy
o lymphoma
o Chaga’s disease-cause by kissing bug that transmit trypanosoma cruzi ESOPHAGEAL SPASM
CLINICAL FEATURES  Episodes of dysphagia and chest attributable to abnormal esophageal
o affects all ages and sexes contractions with normal deglutitive LES relaxation
o early dysphagia on both liquid and solids  dysfunction of inhibitory nerves
o dysphagia worsen by emotional stress and hurried eating Manometric measurement
o course is usually chronic, with progressive dysphagia and weight loss over  uncoordinated (“ spastic”) activity in distal esophagus
months to years  prolonged duration and repetitive contraction
o relieved by increased intraesophageal pressure (i.e., valsalva maneuver,  diffuse contractions
raising the shoulder during swallowing)
o •regurgitation and pulmonary aspiration 2 Variants based in manometry
•acid reflux symptom (heart burn) is against 1. Spastic nutcracker
Achalasia o Extraordinarily vigorous and repetitive contractions with normal
DIAGNOSIS peristaltic onset
RADIOLOGIC 2. Diffuse Esophageal Spasm (DES )
Chest X-ray o Similar but primarily defined by a rapid propagation at the onset of the
•Tubular mediastinal mass beside the aorta contraction and with poor prognosis
•Absence of the gastric air bubble Clinical Feature:
Barium Swallow  Chest pain, retrosternal, long duration
•Esophageal dilatation proximal to the Achalasia  Occurs at rest , during swallowing,
•BIRD BEAK like narrowing at the terminal
 emotional stress
esophagus
 Dysphagia with solid food
•Diagnostic tool of choice
Diagnosis:
CCK (Cholecystokinin) test
 “Cork-screw esophagus” on barium
 normally, CCK causes mild contraction of LES and a more pronounced swallow
release of inhibitory neurotransmitters in the esophageal wall relaxes the  Manometry
sphincter pressure due to the predominant effect of the inhibitory Treatment:
neurotransmitters
 Nitrates, Ca channel blocker before meal
 in patients with achalasia, the stimulatory effect is unopposed, hence the
 Reassurance and anti-anxiety medicines
LES contracts with CCK
Manometry SCLERODERMA ESOPHAGUS

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 Systemic sclerosis with esophageal involvement  chronic cough laryngitis pharyngitis morning hoarseness dental decay
 Atrophy and fibrosis of smooth muscle region of the esophagus sinusitis
 CREST syndrome  Recurrent reflux may cause:
o Calcinosis, a. asthma chronic obstructive pulmonary disease
o Raynaud’s phenomenon, b. bronchitis
o Esophageal dysfunction, c. pneumonia
o Sclerodactyly, d. pulmonary fibrosis
o Telangiectasia) Complications
 End result is hypomotility: failure of muscle contraction in the distal 1. Inflammation
esophagus and incompetency of LES 2. Barrett’s esophagus (pre-cancerous)
 Reflux symptom and dysphagia is common 3. Adenocarcinoma
Barium swallow 4. Stenosis
o dilatation and loss of peristaltic 5. Ulcer reflux
contractions in the smooth muscle portion Diagnosis
of the esophagus 1. History alone
o LES is patulous (relaxed) 2. Therapeutic trial (PPI BID x 7 days)
o Manometric finding is aperistalsis of the 3. Endoscopy
smooth muscle region and hypotension of 4. Mucosal biopsy
LES 5. pH monitoring
o Dietary adjustments (soft food) and 6. Bernstein test/Acid perfusion test
treatment cannot reverse the disease 7. Barium swallow
o Treatment of reflux Treatment
GOAL: provide symptom relief, heal erosive esophagitis, prevent complications
GASTROESOPHAGEAL REFLUX 1. Lifestyle modification
 weight reduction, head of bed elevated about 4-6 inches, elimination of
DISEASE (GERD) factors that increase abdominal pressure
 One of the most prevalent GI disorder:  avoid smoking, fatty foods, coffee, chocolate, alcohol,
15% of individuals have  mints, citrus fruits, too sweets, and medications that
heartburn/regurgitation symptom at least  relaxes smooth muscle
once a week, while 7% have daily  avoid lying down after eating; should eat 4 hours before lying down
symptom. 2. Medication
 Normal antireflux mechanism: lower  Antiacid
esophageal sphincter (LES), crural  H2 receptor blocker (Ranitidine, Famotidine, Cimetidine, Nizatidine)
diaphragm, anatomic location of the CE Proton-pump inhibitor
junction below the diaphragmatic (drug of choice)
hiatus  (Omeprazole, Rabeprazole, Pantoprazole, Esomeprazole, Lansoprazole)
 Cause by loss of pressure gradient 3. Antireflux surgery
between the stomach and LES  fundoplication ( gastric fundus is wrapped around the lower esophagus)
- Decrease LES pressure BARRETT’S ESOPHAGUS
- Increase Gastricpressure o Metaplasia of esophageal squamous epithelium
- Incompetent diaphragmatic to specialized columnar epithelium
crural muscle o Specialized metaplastic columnar epithelium
Three dominant mechanism of - mosaic of different epithelial cells, including
esophageal junction incompetence: goblet cells and columnar cells.
 Trancient LES relaxation (vasovagal o Risk factor for esophageal adenocarcinoma
reflex) o Endoscopically divided into long segment
 LES hypotension (>2-3 cm) and short segment (<2-3cm)
 Anatomic distortion of EG junction (hiatal hernia) o Long segment has higher risk of cancer
Conditions with Decrease LES pressure development
 Scleroderma o Histopathologically divided into high grade
 myopathy dysplasia and low grade dysplasia
 pregnancy
 Diagnosed through endoscopy and biopsy
 smoking Treatment:
 anticholinergic drugs
 High grade dysplasia esophagectomy, endoscopic mucosal resection,
 esophagitis
photodynamic therapy
 surgical damage to LES
 No dysplasia and Low grade dysplasia monitor through follow-up
 fatty meals beverages with a high xanthine content (tea, coffee,
endoscopy barrettsendoscop
cola)
 smooth muscle relaxants: (B-adrenergic blockers, calcium channel
blockers, aminophyline, nitrates, phosphodiesterase inhibitors)
Conditions with Increase gastric pressure
 increase gastric volume (after meals, pyloric obstruction, gastric
stasis, during acid secretion states)
 gastric contents are near the GE junction (recumbency, bending
down, hiatal hernia)
 obesity
 pregnancy
 ascites
 tight clothes
Incompetent diaphragmatic crural muscle
 hiatal hernia
Classification:
o Non-erosive reflux disease(NERD) - mucosa appears normal
o Reflux esophagitis/GERD - develops when mucosal defense are unable to
counteract the damage caused by acid, pepsin and bile
1. Mild esophagitis - involves microscopic changes of mucosal infiltration
with granulocytes or small number of eosinophils
2. Erosive esophagitis - gross mucosal damage with redness, friability,
superficial ulcers and exudates
Clinical Features
 Heart burn or pyrosis (may radiate to the sides of the chest, neck, angles
of jaw). Aggravated by bending forward, straining, or lying recumbent and
worse after meal.
 Regurgitation of sour material in the mouth
 Angina-like or atypical chest pain
 Dysphagia/Choking-like sensation
 Extraesophageal manifestation

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Clinical Manifestations:
ESOPHAGEAL RINGS a. Dysphagia,
b. regurgitation,
Located at the distal esophagus c. choking,
A-Ring (muscular) d. aspiration,
 Symetrical band of hyperthropied e. voice changes,
muscle that’s constricts the tubular f. halitosis,
esophageal lumen g. weight loss
 Located roughly 2cm proximal to Barium swallow is the most useful
the squamo columnar junction diagnostic study
 Consist of three layers:
Treatment :
 mucosa,
 Surgical diverticulectomy and
 submucosa, and
cricopharyngeal myotomy for large
 muscularis propia
sized diverticula ( > 5 cm)
 Covered by squamous cell
 Marsupialization procedure in which
epithelium
an endoscopic stapling device is used
 Dysphagia to solid and liquid
to divide tha cricopharyngeus for
 Bouginage/dilatation or botulinum toxin injection medium sized (2-5 cm)
B-Ring Schatzki Ring  Follow-up for small size
 Common  Other diverticulum
 Thin membrane that constricts the esophageal lumen located at the 1. Midesophageal diverticulum
squamocolumnar junction - caused by traction from old
 Consist of squamous epithelium on its upper surface and columnar adhesions or by propulsion
epithelium on its lower surface (demarcates the squamocolumnar junction) associated with esophageal motor
 Always associated with hiatal hernia abnormalities.
 Composed of - True diverticula involving all
 mucosa and layers of the esophageal wall
 submucosa 2. Epiphrenic diverticulum
 Mostly asymptomatic - may be associated with achalasia.
 Intermittent dysphagia - Small or medium-sized diverticula,
 Diagnosed by esophagogram or endoscopy midesophageal and Epiphrenic
 No treatment required if asymptomatic diverticula are usually
 Bouginage/ baloon dilatation asymptomatic.
- False diverticula
3. Diffuse intramural diverticulosis of the esophagus - due to dilation of the
deep esophageal glands and may lead to chronic candidiasis or development
ESOPHAGEAL DIVERTICULA
of stricture high up in the esophagus
 Outpouchings from tubular structures.
 True diverticula - involves the whole layer of the GIT wall (congenital lesions) TUMORS
 False diverticula - involves the mucosa and submucosa only through the Esophageal cancer
muscular wall (acquired lesions)  Rare but lethal
Zenker’s diverticulum  Incidence show a shift of dominant esophageal cancer type from squamous
 acquired (false diverticula) cell to adenocarcinoma, strongly linked to reflux disease and Barretts
 appears in the natural zone of weakness metaplasia
 result from increase intraluminal pressure associated with distal obstruction  The typical presentation is progressive solid food dysphagia and weight loss
 in the posterior hypopharyngeal wall  Poor survival even if detected as a small lesion, because of the abundant
(Killian’s triangle)- most commonly occurs in this area esophageal lymphatics leading to regional lymph node metastases
Benign esophageal tumors
 Kilians triangle is located where the transverse fibers of the cricopharyngeal
sphincter intersects with the oblique fibers of the inferior pharyngeal  Are uncommon and usually discovered incidentally
constrictor.  Cell types ( in decreasing order of occurrence) : leiomyomas, fibrovascular
neurofibromas and inflammatory fibroid polyps
 Symptomatic only when they are associated with dysphagia and merit
removal only under the same circumstances

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EIOSINOPHILIC ESOPHAGITIS (EoE) Viral Esophagitis

 Increasing incidence in adult and children worldwide Herpes simplex virus (HSV) type 1 & 2
 Diagnosed based on the combination of typical esophageal symptoms and - vesicles on the nose and lips provides diagnosis
esophageal mucosal biopsies demonstrating esophageal squamous Diagnostic confirmation
epithelial infiltration with eiosinophils o endoscopy shows vesicles and small,
discrete, punch- out (volcano-like),
 Common esophageal symptoms: food impaction and dysphagia
superficial ulceration with or without a
 Atopic history of food allergy, asthma, eczema, or allergic rhinitis is
fibrous exudate (early stage) - later
present in the majority of patients
stages show diffuse erosive
 Cytokines such as IL-5, eotaxin, and thymus and activation-related esophagitis that develop from
chemokine (TARC) may be elevated in the serum enlargement and coalescence of
 Characteristic endoscopic findings: ulcers
 Multiple esophageal rings o mucosal biopsy/cytologic smear
 Linear furrows o (Cowdry type A) - ballooning
 Punctuate exudates degeneration, ground- glass
 Histologic confirmation is made with the demonstration of increased appearance changes in the nuclei with
eosinophils in the esophageal mucosa (15 eosinophils per high power eosinophilic intranuclear inclusions
field) o HSV culture
 Fibrosis narrow caliber esophagus, and stricture can occur with EoE o PCR assays are more sensitive than viral culture
 Treatment for EoE include Treatment
- Dietery restrictions, o spontaneous resolution may occur for 1-2 weeks
- PPIs o anti-HSV agents Acyclovir, Valacyclovir, Forcarnet (for Acyclovir
- Systemic or topical glococorticoids (Fluticason propionate or resistant)
budesonide, montelukast, immunomodulatores, and endoscopic Varicella Zoster Virus (VZV)
dilation of strictures) o associated with Herpes Zoster
ESOPHAGEAL FOREIGN BODY o difficult to distinguish from HSV
Levels of Narrowing o treated with Acyclovir or Valacyclovir and may be used in combination
1. Upper esophageal sphincter with steroids
2. Aortic arch Cytomegalovirus (CMV)
3. Left mainstem bronchus o occur only in immunocompromised
4. Diaphragm o diagnosis requires endoscopy and
5. Lower esophageal sphincter biopsy from ulcer base
Treatment: Endoscopic removal o giant ulcers with histologic finding of
HIATAL HERNIA intranuclear and small
intracytoplasmic inclusions in large
 Herniation of the part of stomach into
fibroblast and endothelial cells
the thoracic cavity through the
o immunohistology with monoclonal
esophageal hiatus in the diaphragm
Sliding hiatal hernia antibodies and in situ hybridization
test to CMV are helpful in early
 the GE junction and fundus slide upward
stages
 Common in individuals in the sixth o Ganciclovir is the treatment of choice
decade of life; 60% prevalence
o Foscarnet is used for resistance cases
 Causes reflux esophagitis Bacterial
Paraesophageal hernia o rare, occurs in the immunocompromised patients,
 the GE junction remains fixed in its o i.e.. granulocytopenia, cancer, AIDS patients
normal location and a pouch of stomach o B-hemolytic streptococci, Lactobacillus,
herniates besides the GE junction o Mycobacterium tuberculosis
through the esophageal hiatus
 Hernia may incarcerate and treatment is
PILL-INDUCED ESOPHAGITIS
surgical repair  Antibiotics: doxycycline, tetracycline, minocycline, penicillin, clindamycin
 Hiatal hernias may be classified into one  NSAID: aspirin, indomethacin, ibuprofen
of four types.  Biphosphonates: alendronate, pamidronate
 Type I (sliding hiatal hernia) in which there is a migration of the  Others: potassium chloride, ferrous sulfate, quinidine, theophylline, ascorbic
esophagus-gastric junction above the diaphragm into the thorax is the acid, pinaverium bromide
most common.  Can be avoided by taking pills in upright position and with copious amount of
 Type II is a true paraesophageal hernia in which the stomach herniates fluids
into the thorax, but the esophagus-gastric junction remains fixed in its CORROSIVE ESOPHAGITIS
normal anatomic location below the diaphragm.  Caustic agents: Acid and Alkali
 Type III (mixed Para esophageal hernia) is a combination of a sliding  Acid - HCl (toilet bowl cleaner,
hiatal hernia with some or all of the stomach herniating above the metal cleaner, pool cleaner,
esophagus-gastric junction. antirust) Sulfuric acid (battery
 Type IV are those hiatal hernias which include abdominal viscera and/or fluids)
solid organs within the hernia sac. Rarely, a parahiatal hernia, where  causes immediate pain hence
gastric herniation occurs through a diaphragmatic defect separate from expelled rapidly
the hiatus, may be seen.  coagulation necrosis
INFECTIOUS ESOPHAGITIS  limited penetration and injury to
 Common symptoms:: esophagus
a. odynophagia,  Alkali - lye (strong alkali)
b. dysphagia, - bleaching products, button batteries, drain cleaners, dish washing
c. chest pain detergents
 Causes ulcer in the esophagus - usually odorless and tasteless hence may be swallowed before protective
 Usually found in immunocompromised patient reactions are invoked - liquefaction necrosis - can penetrate the whole
Esophageal Candidiasis thickness of the esophageal wall
 normal commensals in the throat (yeast) species :  Severe injury leads to esophageal perforation, bleeding and death
Candida albicans  Glucocorticoids have no role in corrosive esophagitis
 can be pathogenic in immunocompetent and  Healing is associated with stricture formation which is usually long and
immunocompromised host rigid
 endoscopically shows small, yellow-white raised  Stricture requires esophageal dilatation
plaques with surrounding erythema shows mild  Extensive corrosive damage require esophageal diversion and
disease excision of damage portion
 confluent linear and nodular plaques reflect
extensive disease
 demonstrates yeast or hyphal forms in plaque smears and exudates stained
with periodic acid- Schiff or Gomori silver stains
Treatment:
o oral Fluconazole (200mg 1st day then 100mg daily) for 7-14 days
o others - Itraconazloe, intravenous anti-fungal
o (Echinocandin, Amphotericin B)

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MECHANICAL TRAUMA  History of allergic disease or mild peripheral eosinophilia is present in about
Esophageal Rupture: half of patients.
1. Iatrogenic damage  Barium esophagogram may show a small-caliber esophagus, isolated
2. Boerhave’s syndrome esophageal narrowing, or single or multiple esophageal rings.
 spontaneous rupture due to pressured vomiting and retching  Diagnosis is confirmed by esophageal mucosal biopsies that show
 perforation increased eosinophils (>15) per high-power field or eosinophilic micro
 severe retrosternal chest pain, subcutaneous emphysema, tactile and abscesses.
auscultatory crepitous, pneumothorax  Treatment: inhaled or oral steroids
 secondary infection and mediastinal abscess may occur  Dietary management involves identification of the offending food and its
 CT scan most reliable tool to detect mediastinal air elimination from the diet or a trial of elemental diet for 4 weeks.
 diagnosis is confirmed by swallowing of radiopaque contrast
material
 treatment includes esophageal and gastric suction and parenteral
antibiotics
 Surgical repair and should be performed immediately
MALLORY-WEISS TEAR
 Mucosal tear
 Caused by vomiting, retching or vigorous coughing
 Involves the gastric mucosa near the squamocolumnar junction (Z-line)
 Presents as upper GI bleeding
 Diagnosed by endoscopy
 Bleeding spontaneously stops in most patients

EOSINOPHILIC ESOPHAGITIS
 Hypersensitivity reaction Inflammation and submucosal fibrosis due
eosinophilic infiltration

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