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114 Cards in this Set

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Considered an alarm symptom and should have immediate evaluation at any age.
dysphagia
d
the three classifications of dysphagia:
oropharyngeal, esophageal, functional
o,e,f
“transfer dysphagia”
arises from diseases of the upper esophagus, pharynx, or UES dysfunction
Complaint: Usually described as difficulty immediately upon swallowing. Patient will usually point to cervical region.
oropharyngeal dysphagia
o d
Usually arises from within the body of the esophagus, the LES, or cardia.
Most commonly due to mechanical causes or motility disorders.
esophageal dysphagia
e d
a type of esophageal dysphagia: events of swallowing are poorly coordinated or muscles fail to relax to allow passage of food
Intermittent, equal difficulty with solids and liquids
motility dysphagia
m d
A type of esophageal dysphagia: diameter of esophageal lumen must be narrowed to less than 1.3 cm. Swallowing is typically worse for solids than liquids
It is the usual presentation of esophageal cancer
obstructive/mechanical dysphagia
o/m d
intermittent burning, substernal chest pain
Injury to esophageal epithelium by reflux of acid
pyrosis
p
pain is triggered by swallowing
Usually accompanies severe esophageal inflammation
odynophagia
o
Procedure of choice for diagnosis of esophageal mucosal diseases
Allows direct visualization of entire mucosa of esophagus
Permits biopsy, injection or cautery of lesions, dilation of strictures, extraction of foreign bodies
endoscopy
e
Provides information on anatomy of esophagus and its motor function.
Series of radiographs obtained by fluoroscopy while patient is swallowing liquid barium contrast material
Pictures taken while in upright and supine positions
Barium Esophagram (Barium swallow or Upper GI X-ray)
b e
Used for oropharyngeal dysphagia
Typically performed by speech pathologist and radiologist
Patient swallows a variety of foods covered with barium
Video fluoroscopic recording is made in AP and lateral views
Allows observation of bolus progression through the different stages of swallowing
Video Fluoroscopic Swallowing Study (Modified barium swallow)
v f s s (m b s)
Information regarding esophageal wall and surrounding mediastinum
Useful for staging esophageal cancer
Transesophageal ultrasound used to evaluate submucosal and extramural lesions
CT, MRI, Endoscopic US
c, m, e
Identify and characterize disorders of esophageal motility
Flexible tube with _________ probe is passed thru nasopharynx, swallowed by patient, enters stomach. Probe measures pressures (amplitude and duration of contraction).
Provides assessment of lower and upper esophageal sphincters and integrity of esophageal peristalsis.
manometry, esophageal manometry
m, e m
pH probe introduced through nasopharynx
Function of LES assessed

Bernstein test
24 hour pH monitoring
esophageal pH monitoring
e p m
Small amounts of fluid are infused through probe to reproduce chest pain and discomfort.
Hydrochloric acid and salt water are used.
Used to reproduce symptoms of heartburn
Bernstein test (Acid perfusion test)
b t (a p t)
Continuous readings of distal esophageal pH over 24 hours can be recorded by computer to determine frequency of reflux events and effectiveness of peristaltic acid clearance.
Useful to document periods of LES relaxation that lead to gastroesophageal acid reflux.
pH levels are compared to patient’s record of symptoms
24 hour pH monitoring
# h p m
Most common: 85-95% upper esophagus ends in blind pouch and lower end of esophagus enters trachea just above its bifurcation
Congenital Tracheoesophageal Fistulas and Esophageal Atresia
c t f and e a
Clinical Presentation:
Infants present with excess saliva production from inability to swallow.
Choke and cough when oral feeding is attempted.
Cyanosis or pneumonia can occur from feedings or GI secretions that are aspirated into lungs.
Diagnostic:
Barium esophagram
CT scan
Treatment:
Surgery
Congenital Tracheoesophageal Fistulas and Esophageal Atresia
c t f and e a
Usually a complication of esophageal or bronchogenic carcinoma

Formed when tumor invades adjacent structure and undergoes necrosis
acquired tracheoesophageal fistula
a t f
Clinical Presentation:
Aspiration of saliva and food when patient swallows.
Rapidly leads to severe, often fatal pneumonia.
Diagnostic:
Barium esophagram
Treatment:
Surgery impossible if cancer in airway and esophagus
Treatments aimed at shrinking tumor usually enlarges fistula
Palliative treatment: stent esophageal lumen to permit passage of food while blocking opening of fistula
acquired tracheoesophageal fistula
a t f
Gastroesophageal junction and fundus of the stomach slide upward
Stomach slides up and down thru hiatus
Incidence increases with age, usually in 60’s
sliding hiatel hernia (type 1)
s h h
Clinical Presentation
95% of presenting hiatal hernias
Usually asymptomatic & harmless
May develop GERD
Diagnostic
Barium esophagram
Endoscopy to visualize Z line (squamocolumnar junction) and gastric folds above diaphragm
Treatment
Surgery reserved for those with severe GERD or hernias greater than 8-10 cm (differs according to surgeon)
sliding hiatel hernia (type 1)
s h h
Esophagogastric junction remains fixed in normal position while stomach rolls up along side lower esophagus
Stomach herniates through a diaphragmatic defect
paraesophageal hiatal hernia (types II, III, IV)
p h h
)a type of hernia)
Clinical Presentation
Dyspepsia, pyrosis, bloating
If hernia is massive, obstructive symptoms can occur due to angulation and compression
Diagnostic
Barium esophagram
Endoscopy
paraesophageal hiatal hernia (types II, III, IV)
p h h
Never regress and progressively enlarge.
If left untreated, eventually reaches the stage of a giant intrathoracic stomach (prognosis is poor and the complication rate is high)
Complications: gastric volvulus, bleeding (Cameron lesions- erosions within the incarcerated hernia pouch), strangulation, infarction of incarcerated stomach, and respiratory compromise (mechanical compression from hernia).
Should be treated surgically even in the absence of symptoms
paraesophageal hiatal hernia (types II, III, IV)
p h h
Posterior outpouching of mucosa/submucosa just above the UES

Food may collect in pouch
Regurgitation or aspiration of undigested food hours after eating is a useful clue to diagnosis
Diverticulum may compress the upper esophagus and occlude the lumen
Often discovered incidentally when performing upper GI for other reasons
Zenker's diverticulum
z d
Clinical Presentation
Dysphagia, foul breath, neck pain, swelling
Usually > 60 yo but have had symptoms for years
Regurgitation of undigested food when patient bends over or lies down
May lead to aspiration pneumonia
Diagnostic
Barium esophagram
Treatment
Asymptomatic – nothing done
Surgical diverticulectomy
Zenker's diverticulum
z d
Rare, was caused by contraction of scars from tuberculosis
Clinical Presentation
Chest pain, dysphagia, aspiration
Diagnostic
Barium esophagram
Endoscopy
Treatment
Surgery
mid-esophageal diverticulum
m-e d
Esophageal Diverticula
common in what three places
Zenker’s diverticulum
just above UES
Mid-esophageal diverticulum
mid esophagus at level of aortic arch
Epiphrenic diverticulum
distal esophagus just above LES
z d, m-e d, e d
a type of diverticula:
Found in the last 5-10 cm of the esophagus immediately proximal to the LES
Clinical Presentation
Chest pain, dysphagia, aspiration
Diagnostic
Barium esophagram
Endoscopy
Treatment
Surgery
epiphrenic diverticulum
e d
Thin, esophageal circumferential ring occurring at the gastroesophageal junction (GE junction)
Ring covered with squamous mucosa above and columnar epithelium below.
Central core is composed of vascular fibrous tissue
Cause is controversial & thought to be due to GERD, congenital or developmental deformity
Schatzki's Ring
s r
Clinical Presentation
Dysphagia to solids is only symptom and usually occurs episodically
Large food boluses may become impacted in the ring and cause abrupt onset of complete esophageal obstruction with substernal discomfort
Patient usually complains of choking but airway is not involved – breathing and speech are unaffected
Schatzki's Ring
s r
Diagnostic
Barium esophagram
Endoscopy may be required to dislodge and remove bolus
Treatment
Bougienage or balloon to dilate ring mechanically to prevent further episodes
If ring thought to be due to GERD, PPI is indicated.
Schatzki's Ring
s r
Strictures treated by forcible dilation
Strictures frequently recur if GERD is not controlled
bougienage
b
Mucosal fold that protrudes into the lumen covered with squamous epithelium
Typically protrudes from the anterior wall in the cervical esophagus
Etiology remains unknown
esophageal webs
e w
Clinical Presentation
Intermittent dysphagia to solids
Classically symptomatic webs in iron-deficient, middle-aged women constitute Plummer-Vinson syndrome
Iron supplements may cause web and dysphagia to disappear.
However, one study showed no correlation between esophageal webs and iron deficiency
Diagnostic
Barium esophagram with lateral view
Treatment
Bougienage or balloon to mechanically rupture web
esophageal webs
e w
Presents as an inability to swallow saliva or acute onset of dysphagia
Usually occurs after eating a large bolus of meat
Do not allow impaction to remain > 24 hours due to increased risk of perforation
esophageal foreign body
e f b
Diagnostic
Plain neck, chest, and/or abdominal radiographs may reveal a radiopaque foreign body or signs of esophageal perforation such as mediastinal, subdiaphragmatic, or subcutaneous air.
Radiographic localization and identification of foreign bodies in the esophagus is important prior to any attempt at extraction.
Do not do a barium swallow.
Protect the airway.
Give continuous oropharyngeal suction as needed to avoid pulmonary aspiration.
esophageal foreign body
e f b
Diagnostic
Complete obstruction requires immediate intervention.
Food bolus should not remain in esophagus for >12 hours to avoid pulmonary aspiration.
All patients should be evaluated for esophageal rings and stricture after the FB is removed (this is the most common cause of esophageal body obstructions in adults).
Treatment
Glucagon 1 mg IV can be given in attempt to relax the esophagus and pass the bolus. (usually not helpful)
A benzodiazipine can be given to help relax the patient if overly anxious.
Endoscopy (TOC) if medication treatment fails
food
f
35% or more of children are asymptomatic

Diagnostic
Esophageal coin is visible on AP CXR as a disk
Tracheal coin tends to be on edge
Treatment
Endoscopy is treatment of choice
If in the stomach, no need for retrieval
coin
c
Medical emergency
May have perforation in 2 hours

Treatment
Requires endoscopic retrieval if lodged in the esophagus
If in stomach, watch for 24-48 hours to see if it passes, if not, must be removed endoscopically
button battery ingestion
b b i
Drug smugglers ingest plastic or latex packets filled with cocaine or narcotics
Rupture of packets may be fatal causing local intestinal ischemia or systemic cocaine intoxication
Packets are usually radiopaque
Progress is monitored by daily abdominal films
body packer
b p
If package stops moving through the GI system or the patient develops symptoms – surgical removal is needed
Endoscopy is contraindicated secondary to risk of perforating packets
body packer
b p
Autoimmune disorder that deposits collagen in the skin and viscera
May develop CREST syndrome
Calcinosis
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Atrophy and fibrous replacement of smooth muscle in the muscularis propria of the distal esophagus results in weakness of contraction in the lower 2/3 of the esophagus and incompetence of LES
scleroderma
s
spider veins
telangiectasias
t
(found with scleroderma) a localized thickening and tightness of the skin of the fingers or toes. Commonly associated with atrophy of the underlying soft tissue
sclerodactyly
s
Clinical Presentation
Dysphagia to solids
Pyrosis and regurgitation
Develop severe GERD
Diagnostic
Barium esophagram shows dilation and loss of peristaltic contractions in middle and distal portions of the esophagus with loss of LES tone
GERD may occur freely
Treatment
Aggressively treat GERD and underlying disease
scleroderma
s
*******
Greek term that means: “does not relax”

Characteristics :
loss of peristalsis in the distal esophagus
failure of LES to relax
dilatation of the esophagus
achalasia ********
a
Normal peristalsis is lost
Food accumulates in the esophagus, distending and dilating it
Esophagus empties by Hurst phenomenon
it fills with fluid until the pressure of the column is greater that the LES, then the LES is forced open allowing contents to flow into stomach until LES closes again
Currently unknown if it increases risk for cancer
achalasia
a
Etiology
Unknown
In US almost always idiopathic – but can be due secondarily to carcinoma and irradiation
FYI: In South America, usually from Chagas’ disease (Trypanosoma cruzi)
Neurotoxin destroys nerve endings in the myenteric plexus of the distal esophagus
achalasia
a
Presenting age usually 25-60 years old
M = F
Uncommon disorder
Dysphagia to solids and liquids
Evolves insidiously over months to years
Regurgitation of undigested food
GERD
Retrosternal chest pain from esophageal spasms
Weight loss (affects appetite)
Hiccups (vagus nerve is stimulated)
achalasia
a
Barium esophagram
massive dilated esophagus with smooth, tapered “Bird’s beak” narrowing at the level of the LES
Fluroscopy shows that normal peristalsis is lost in the lower 2/3 of the esophagus
achalasia
a
Endoscopy usually reveals no specific mucosal abnormality but can exclude malignant neoplasm
however, malignant tumors are infiltrative and not easily detected
Esophageal manometry is definitive study
Absent distal peristalsis
Elevated resting LES pressure
Incomplete LES relaxation
Elevated baseline esophageal pressures
achalasia
a
3 basic treatment modes
1. Symptoms can be relieved with smooth muscle relaxants
NTG SL, before meals and at bedtime
Isosorbide dinitrate PO, before meals
Nifedipine SL (CaChBlocker), before meals
2. Endoscopic injection of botulinum toxin (BOTOX) into the LES induces prolonged paralysis of this muscle and may relieve symptoms for months
(30-50% response rate)
3. Definitive treatment is disruption of LES by pneumatic dilation (70% response rate) or by surgical myotomy (cut muscle of LES) (90% response rate)
achalasia
a
surgery where muscle fibers of the LES are cut and used in the treatment of achalasia
myotomy
m
a phenomenon associated with esophageal emptying:
it fills with fluid until the pressure of the column is greater that the LES, then the LES is forced open allowing contents to flow into stomach until LES closes again
Hurst phenomenon
h p
Frequent, abnormal, nonpropulsive esophageal contractions that can be simultaneous, repetitive, prolonged or of unusually high amplitude
Normal peristalsis is also present some of the time
Etiology is unknown
diffuse esophageal spasm
d e s
Chest pain, dysphagia or both
Chest pain assoc with esophageal dysmotility:
is precipitated by drinking cold liquids or stress
is retrosternal and may radiate to the back, sides of chest, both arms, jaw
may be acute, severe and mimic an MI
Intermittent dysphagia that is equal for solids and liquids
Correct diagnosis often difficult to make
diffuse esophageal spasm
d e s
diagnostic:
Exclude coronary artery disease 1st
Barium esophagram may reveal nonpropulsive contractions or diffuse esophageal spasms “corkscrew esophagus”
diffuse esophageal spasm
d e s
treatment:
Symptoms may be relieved with smooth muscle relaxants (not very effective)
NTG : before meals and at bedtime
Isosorbide dinitrate: before meals
Nifedipine SL: before meals

* Remind pts that this may drop their blood pressure, so use caution.
diffuse esophageal spasm
d e s
Dysphagia characterized by poor coordination of skeletal muscle in oropharynx, UES, and proximal esophagus
Patients often regurgitate or aspirate when initiating a swallow
Liquids are especially a problem – sometimes being expelled from the nose or triggers coughing (good clinical question to ask)
Clinical term “oropharnygeal dysphagia”
dysphagia associated with neuromuscular disorders
Cerebrovascular Accident
Parkinson’s
Myasthenia gravis
Botulism
Muscular dystrophy
Polymyositis
d a w/ n d
Diagnostic
Swallow study with flouroscopy and barium esophagram, usually done by speech pathologist and radiologist
Treat underlying disorder
Often unsuccessful
Can lead to aspiration pneumonia so many patients need a gastrostomy tube
dysphagia associated with neuromuscular disorders
Cerebrovascular Accident
Parkinson’s
Myasthenia gravis
Botulism
Muscular dystrophy
Polymyositis
d a w/ n d
Increased tone in the UES with incomplete relaxation
Common under conditions of grief
Leads to perception of “lump in the throat”
Can be persistent in patients with anxiety
Diagnostic
Imaging and physiologic studies are typically normal
Treatment
Reassurance and relief of anxiety
globus sensation
g s
Unusual disorder characterized by incomplete relaxation of UES and impaired food passage

Failure of cricopharyngeal muscle to relax with pharyngeal contraction
closes off opening of esophagus
cricopharyngeal achalasia
c a
“Sticking” of food at level of cricoid cartilage
Dysphagia of liquids and solids equally
May cause aspiration
cricopharyngeal achalasia
c a
Barium esophagram
demonstrates enlarged cricopharyngeal muscle that fails to relax due to hypertrophy or neuromuscular dysfunction
cricopharyngeal achalasia
c a
Dilatation
Occasionally requires surgical disruption of cricopharyngeal muscle to relieve dysphagia
May develop pulsion diverticulum (Zencker’s) secondarily
cricopharyngeal achalasia
c a
Also called reflux esophagitis

the reflux of stomach and duodenal contents into the esophagus, manifesting as a combination of symptoms and signs.
It occurs when esophageal squamous epithelium suffers prolonged exposure to gastric HCl acid and pepsin from deficiencies of the esophageal reflux barrier and acid-clearing mechanisms
One of the most common GI conditions in clinical practice
GERD
g
etiology:
Normal barriers to reflux and damage:
LES tone
Resistance of esophageal mucosa to acid (salivary pH, esophageal epithelium, and bicarbonate secretions)
Clearing of acid from esophagus
Normal gastric motility (peristalsis)
Quantity and characteristics of gastric fluids produced
GERD
g
clinical presentation:
Pyrosis (heartburn) “hallmark sign”
Pain may be felt in the epigastric area and mistaken for gastric or duodenal ulcer
Frequent spontaneous regurgitation of sour (gastric) contents
Dysphagia
Chronic cough (often at bedtime when lying flat)
Atypical chest pain (CP ruled out as cardiac)
GERD
g
clinical presentation:
May awaken at night after choking on mouthful of gastric juice
Symptoms worse after large, fatty meals
Can cause pharyngitis and/or hoarseness
Nocturnal aspiration of acidic gastric contents can lead to pneumonia, particularly in the elderly
Acid reflux into esophagus can trigger bronchospasm and exacerbate asthma
Can be asymptomatic
GERD
g
Usually diagnosed from history and treated with diet modification and antireflux medication
Endoscopy can confirm the diagnosis, assess severity and eliminate other possible causes
Barium esophagram can show strictures/ulcers
24 hour esophageal pH monitoring (dx when sxs correlate with pH4)
Bernstein test (tests sensitivity to HCL vs normal saline)--
GERD
g
treatment:
Goal is to relieve and prevent symptoms and complications
Lifestyle modifications
Medical
Surgical
Endoscopic Therapies (FDA approved for safety, but not efficacy)
GERD
g
general measures:
elevate head of bed 6 inches (adding pillows does not work – increases intraabdominal pressure)
avoid tight clothes
lose weight
eat smaller meals
avoid lying down 2-3 hours after eating
avoid reflux-causing foods
avoid alcohol and tobacco (nicotine affects sphincter)
GERD
g
what are these:
Ingestion of fat (slows the motility of the gut)
Pregnancy
progesterone secretion relaxes the LES and the enlarging uterus increases intra-abdominal pressure – accounts for the high frequency of reflux in the 3rd trimester
Gastric intubation
Scleroderma and CREST
due to loss of LES tone and distal esophageal peristalsis
factors that can reduce LES tone
treatment:
Eliminate acid by neutralization, or drug suppression of acid secretion
Antacids (OTC)
Sodium Alginate/antacid combination (OTC)
H2 recepter antagonists (OTC)
Cimetidine, ranitidine, nizatidine, famotidine
Proton pump inhibitors (PPI)
Omeprazole (Prilosec) (OTC), lansoprazole, esomeprazole, rabsprazole
Suppresses acid formation and increases LES tone
Reserved for those unresponsive to H2 blockers
More effective than H2 blockers for long-term control
GERD
g
Alarm symptoms: dysphagia, weight loss
if severe symptoms, don’t hesitate to refer to gastroenterologist
GERD
g
what are these:
Dysphagia
Bleeding
Weight Loss
Choking (acid causing coughing, SOB, or hoarseness)
Chest pain
alarm symptoms of GERD
used in treatment of GERD:
The gastric fundus is wrapped around the esophagus to try and restore sphincter competence.
Restore LES
Reduce reflux
Heal peptic esophagitis
May lead to reversal of peptic stricture
Nissen Fundiplication
n f
Approximately 40% of pts will be free of HB and don’t require medical therapy after prolonged f/u
Approx. 60% will return for medical therapy
Complications due to surgery...
Nissen Fundiplication
n f
Distal 5 cm of esophagus is anchored in the abdomen by wrapping part of the stomach around it
Re-establish the normal anatomic relationships and reinforce the LES
Eliminates reflux and symptoms
Unable to belch and complain of abdominal distention
Nissen Fundiplication
n f
What are these:
Aspiration pneumonia
Acid laryngitis
Trigger asthma
Pulmonary fibrosis
Stricture formation
Barrett’s esophagus with predisposition to adenocarcinoma
complications from GERD
Due to chronic reflux
Men>Women
Chronic damage to lower esophagus tissue can cause replacement of the native squamous epithelium with metaplastic columnar epithelium.
Eventually can result in low or high grade dysplasia
Associated with adenocarcinoma
Barrett's esophagus
b e
treatment:
Normalization of acid in the esophagus has shown to decrease cell proliferation .
It is unknown how much acid control is needed and for how long (studies pending).
Treat with a PPI until results of studies are known. (not H2)
Barrett's esophagus
b e
Ingestion of caustic agents
Involvement is usually patchy and can extend from the oropharynx to the stomach
Can lead to ulceration, necrosis and perforation in severe cases requiring surgery
Healing may be assoc with fibrosis and stricture formation
Strictures also increase the risk of squamous cell carcinoma
Dilate strictures if present
corrosive esophagitis
c e
Usually due to direct, prolonged mucosal contact
Most Common:
NSAIDS
KCL pills
Quinidine
Zalcitabine
Zidovudine
Alendronate
Risedronate
Iron
Vitamin C
Abx: Doxycycline, tetracycline, clindamycin, Bactrim
medication-induced ulcers/esophagitis
m-i u/e
Sxs:
Severe retrosternal chest pain
Odynophagia
Dysphagia
Chronic injury may lead to:
Severe esophagitis with stricture
Hemorrhage
Perforation.
medication-induced ulcers/esophagitis
m-i u/e
Most commonly occurs in immunosuppressed patients
AIDS
solid organ transplants
Leukemia
Lymphoma
Receiving immunosuppresive drugs (chemo, prednisone, etc.)
clinical presentation:
Dysphagia
Odynophagia
Occasionally substernal chest pain
infectious esophagitis
i e
Predisposed
Immunosuppressed
Systemic abx
Uncontrolled diabetes
Systemic corticosteroids
Radiation therapy
Oral thrush may be absent (present in only about 75% of pts)
Sometimes pts are asymptomatic
candidal esophagititis
c e
diagnositic:
Diagnostic certainty, endoscopy with bx and brushings
Shows diffuse, linear, yellow-white plaques adherent to the mucosa
Branching pseudohyphae on microscopic examination
candidal esophagititis
c e
treatment:
Nystatin suspension
500,000 U/ml, 4-6 ml, swish and swallow 5 times/day
Clotrimazole troches
10 mg dissolved in mouth 5 times/day
Fluconazole (if immunocompromised)
100 mg po q day
candidal esophagitis
c e
Herpes Simplex Virus 1 (HSV1):
Causes multiple small, deep ulcerations

Cytomegalovirus (CMV):
Causes one to several large, shallow, superficial ulcerations.
viral esophagitis
v e
which viral esophagitis:
Immune-competent pts can be tx symptomatically and generally do not need antiviral therapy.
Immunosuppressed
Acyclovir (Zovirax)
250 mg/m2 IV q 8-12 or 400 mg orally 5 times/day, usually for 7-10 days
treatment for HSV1
h
which viral esophagitis:
Initial therapy
Ganciclovir
5 mg/kg IV q 12 hours for 3-6 weeks
If condition has improved, but not resolved after full-dose tx it may be continued for an additional 2-3 weeks.
Neutropenia is a frequent dose-limiting side effect
The principal toxicity is renal failure
treatment for cytomegalovirus
c
Treatment of thoracic cancers with ionizing radiation causes injury to esophagus

Clinical Presentation
Dysphagia and odynophagia
Develops weeks after starting radiation therapy and ends weeks to months after completion
Late complications: scarring and stricture formation

Treatment
Viscous lidocaine
Strictures may be treated with dilation
radiation esophagitis
r e
Pressure in the portal vein rises (portal hypertension) and blood is redirected to the distal esophagus causing dilatation of submucosal veins
Dilated submucosal veins=varices
Found in 50% of pts with cirrhosis
1/3 of pts with varices develop an Upper GI bleed
esophageal varices
e v
Clinical Presentation
Profuse hemorrhage from upper GI source

Diagnostic
Upper endoscopy

Fact
Mortality rate w/i 2 weeks of an acute variceal bleed is 30%
esophageal varices
e v
Injection of sclerosing agent (sclerotherapy) or applying bands (band ligation) during endoscopy
Somatostatin and octreotide infusion reduces portal pressure and can help provide acute control of bleeding in up to %80 of pts
Transvenous Intrahepatic portosystemic shunts (TIPS) (portal decompression) vs surgery
esophageal varices
e v
Vomiting that is prolonged and severe can cause linear, longitudinal lacerations of the mucosal in the region of the esophageal junction
Lacerations are superficial, nontransmural
However, disruption of submucosal artery can cause massive upper GI hemorrhage
Can be seen after an alcoholic binge with violent retching or dry heaves
Mallory-Weis tears
m-w t
treatment:
Conservative management
May inject epinephrine during endoscopy to stop bleeding
Surgery if arterial bleed is severe
Mallory-Weis tears
m-w t
Spontaneous transmural perforation of the esophagus *emergency
Results from a sudden rise in intraluminal esophageal pressure and negative intrathoracic pressure produced during forceful vomiting or retching
Most common tear is located at the left posterolateral wall of the lower 1/3 of the esophagus, 2-3 cm proximal to the gastroesophageal junction
Associated with a high morbidity and mortality
Boerhaave syndrome
b s
Repeated episodes of vomiting, retching
Excess dietary and alcohol intake
Sudden onset of excruciating retrosternal chest pain and upper abdomen pain (classic symptoms)
Other sxs: odynophagia, tachypnea, dyspnea, cyanosis, fever, and shock
Mackler’s triad: vomiting, lower thoracic pain, subcutaneous emphysema (crepitation) (present in 9 out of 34 pts with this syndrome)
diagnositic:
CXR
Barium esophagram with Gastrograffin (water soluble contrast)
Boerhaave syndrome
b s
Mackler's triad
vomiting, lower thoracic pain, subcutaneous emphysema (crepitation)
associated w/ Boerhaave syndrome
v, l t p, s e (c)
vomiting, lower thoracic pain, subcutaneous emphysema (crepitation)
associated w/ Boerhaave syndrome
Mackler's triad
m t
treatment:
Direct repair of the esophagus with adequate drainage of mediastinum and pleural cavity
If diagnosed > 24 hour after perforation consider alternative repair procedures
Boerhaave syndrome
b s
Most frequent benign tumor of esophagus
Small (2-5 cm), solitary, round, firm masses
Arise in the submucosa of distal esophagus
leiomyomas
l
clinical presentation:
Usually asymptomatic, discovered incidentally
May cause dysphagia if lumen is compromised
Seldom bleed
leiomyomas
l
treatment:
Cannot be distinguished from malignant neoplasms unless surgically removed
Endoscopic biopsies not helpful in diagnosis of submucosal tumors
Simple surgical excision
leiomyomas
l
Early detection is difficult
15% of esophageal cancers are in the upper 1/3 of the esophagus
50% are in the middle third
35% are in the lower third
Rate of squamous cell carcinoma staying the same, while the rate of adenocarcinoma is markedly increasing in the last 20 years (more Barrett’s esophagus because of increased obesity)
malignant neoplasms
m n
M>F, incidence increases with age
African American population higher risk than Caucasians
Alcohol and smoking are important predisposing factors
Found in the proximal 2/3 of the esophagus
squamous cell carcinoma
s c c
M>F
Caucasian population higher risk than African American
GERD and Barrett’s esophagus are predisposing factors along with obesity and diet lacking fruits, vegetables and fiber
Found in distal 1/3 of the esophagus
adenocarcinoma
a
clinical presentation:
Progressive dysphagia and weight loss are the most common signs of esophageal cancer
Dysphagia begins with solids and gradually progresses to semisolid foods and liquids
Weight loss from anorexia and dysphagia
Hoarseness from recurrent laryngeal nerve involvement
With total obstruction, food and saliva are regurgitated or aspirated to cause pneumonia
adenocarcinoma
a
diagnosis:
Barium esophagram
“apple-core” lesions
fails to detect 73% of early stage tumors of the head and neck
Endoscopy best for diagnosis
biopsy and cytology for tissue confirmation
CT
assess lymphadenopathy, regional involvement of mediastinal structures and metastases to liver and lung
Endoscopic ultrasound
view of regional lymph nodes
more accurate than CT for assessing depth of tumor invasion
CT
adenocarcinoma
a
Prognosis is poor regardless of therapy
Goal of therapy is local control of disease
Surgical resection (esophagectomy) with radiation and/or chemotherapy
Median survival rate in “curative” resection is 12-15 months
adenocarcinoma
a