Esophageal diseases
Obstruction
Anatomic disorders
esophagitis
varices
tumors
functional #
structural
benign esophageal stenosis (strictures)
esophageal mucosal webs
esophageal rings
protrusions of mucosa + submucosa into the lumen
semicircumferential
upper esophagus
etiology
congenital
acquired
GERD
chronic GVHD
blistering skin diseases
Plummer–Vinson syndrome (PVS) AKA Paterson–Brown–Kelly syndrome = upper esophageal webs + IDA + atrophic glossitis
distal esophagus
protrusions of mucosa + submucosa + sometimes hypertrophied muscularis propria
etiology
conginital
acquired
GERD and Barrett's #
scleroderma
radiation
caustic injury
fibrous thickening of wall, esp submucosa, atrophy of muscularis propria, epithelium is thinned and maybe ulcerated
usually adults complaining of dysphagia
achalasia
hiatal hernia
diverticula
incomplete LES relaxation in swallowing + increased LES relaxation tone + aperistalsis
etiology
primary: loss of intrinsic inhibitory neurons of LES or idiopathic (viral, or autoimmune)
secondary: chagas disease (T.cruzi) destroys myenteric plexus in esophagus, duodenum, colon, and ureter.
poliomyelitis and DM neuropathy affect dorsal motor nuclei.
malignancy, amyloidosis, and sarcoidosis are infiltrative.
pathophysiology
functional obstruction of esophagus
dilation of esophagus above LES
affects young adults most, dysphagia to solids and fluids, nocturnal regurgitation
can be complicated with aspiration and SCC (5%)
crura separation and widening, stomach protrudes through the widening
patterns
axial (sliding) (more common)
bell shaped stomach
non axial (paraesophageal)
regurgitation and heartburn, accentuated by bending forward, lying supine, and obesity.
might be complicated by GERD, mucosal ulceration, bleeding, and perforation
rarely induce reflux
might be strangulated or obstructed, or less commonly ulceration, bleeding, and perforation.
zenker diverticulum
traction diverticulum
epiphrenic diverticulum
pharyngoesophageal, immediately above UES
midpoint of esophagus
immediately above LES
etiology ass/w disordered cricopharyngeus and maybe GERD
can accumulate food, cause dysphagia and food regurgitation, mass in the neck, and high risk for aspiration pneumonia
wall weakening due to TB of mediastinal LN, motor dysfunction, or congenital
asymptomatic
discoordination of peristalsis and LES relaxation
may lead to nocturnal regurgitation
dilated veins in mucosa + submucosa
distal esophagus and proximal stomach (portal-systemic anastomosis)
because of portal HT, as in cirrhosis (hepatitis, alcohol, schistosomiasis)
clinical pic
asymptomatic unless ruptured
when ruptured, massive hematemesis that
subsides spontaneously 50%
25% die during first episode
rebleeding 70% chance within first year, with a similar rate of mortality 25%
Tx
sclerotherapy (thrombotic agent injection
balloon temponade
ligation
inflamation of mucosa
common, esp in Iran and China
caused by
GERD (most common)
(AKA reflux esophagitis)
chemicals (stomach acid, alcohol, corrosives, hot fluids, smoking, pill induced, anticancer CTX (cyclophosphamide) + RTX (ritixumab)
infections (HSV, CMV, candidiasis)
others: uremia, crohn's disease, skind disease, GVHD
inflammation due to acid reflux
adults with recurrent heartburn (dominant symptom) dysphagia, regurgitation, and rarely, chest pain.
etiology
decreased efficacy of antireflux mechanisms
CNS depressants
alcohol
tobacco
prolonged gastric intubation
sliding hiatal hernia
inadequate clearance of refluxed material
delayed gastric emptying
increased gastric volume
mostly idiopathic
gross appearance
depends on the causative agent and duration+severity of exposure to be mild or sever
mild esophagitis: simple hyperemia
severe esophagitis: epithelial erosions or ulceration into submucosa
microscopic appearance
intraepithelial eosinophils, with neutrophils if severe
basal zone hyperplasia
elongation of lamina propria papillae and capillary congestion
severity of symptoms is not closely related to the degree of histologic picture
serious complication: Barrett's esophagus
metaplastic columnar epithelium in esophagus
affects 10% of those with chronic GERD, esp white males
pathogenesis: chronic GERD -> squamous layer inflamation and ulceration -> reepithelialization with columnar layer (origin: from migration of gastric mucosa or growth and differentiation of stem cells)
grossly
salmon pink, velvety
located bw the smooth pink mucosa of esophagus and the brown mucosa of stomach
may exist as
tongues extending up from the GEJ
arregular circumferentail band
isolated patches in distal esophagus
microscopically
columnar metaplasia (contains goblet cells
may be focal requiring repeated endoscopy and biopsy
grading dyspasia is important
complications
barrett's ulcer
stricture (stenosis)
dysplasia and adenocarcinoma #
around 1% of those with barrett per year
higher risk in higher grade of dysplasia
screening is recommended
benign
malignant
SCC (90% of malignant)
adenocarcinoma
leimyoma (most common)
squamous papilloma
black adult males more affected
high incidence in Iran, China, and South Africa
pathogenesis: dysplasia -> CIS -> invasive carcinoma
patterns
polypoid exophytic (most common)
ulcerated and necrotic
diffuse and infiltrative; causes thickening of wall + narrowing of lumen
20% in upper third of esophagus
50% in middle third of esophagus
30% in lower third of esophagus
most important risk factors are alcohol consumption and tobacco abuse, others are here
Barrett's esophagus is the precursor
risk factors
tobacco, obesity, and radiation (no association with alcohol)
whites are more affected
pathogenesis: esophagitis (GERD) -> barrett's (metaplasia) -> dysplasia -> carcinoma
grossly
distal one third of esophagus (like barrett's)
may invade gastric cardia
initially appears as flat or raised patches that develop into large nodular masses or ulcerative of diffuse infiltrative patterns
microscopically
shows mucin producing glandular tumors of intestinal type
clinacally
early asymptomatic
progressive dysplasia and odynophagia
weight loss, anorexia, fatigue, and weakness
diagnosis by imaging techniques and endoscopic biopsy
prognosis is poor, when symptomatic the tumor is large and has already invaded wall, lymphatics, and adjacent structures
stage is the most important prognostic factor
surgical excision is rarely curative