Esophageal Conditions

Kibrom Gebreselassie, MD, FCS-ECSA

Cardiovascular and Thoracic Surgeon
 Benign Esophageal Pathologies
Motility Disorders
Esophageal Carcinoma
Hiatal Hernia
Develops when a lax or defective
phrenoesophageal membrane allows protrusion of
the stomach up through the esophageal hiatus of
the diaphragm.
 Epidemiology
Most common abnormality reported in UGI radiographic
studies.
Most common in women in their fifth and sixth decades.
Most HH are asymptomatic, however 5% of pts have
symptoms associated with GERD.
ANATOMY

95%

1%

4%
 Type of HH
Type I or sliding HH- the phrenoesophageal membrane is
intact but lax, thereby allowing the distal esophagus and
gastric cardia to herniate and placing the GE junction
above the diaphragm.
This is the most common type and is usually
asymptomatic.
 Type II or Paraesophageal HH- occurs when a focal
defect is present in the phrenoesophageal membrane,
usually anterior and lateral to the esophagus, which
allows a protrusion of peritoneum to herniate upward
alongside the esophagus.
 The GE junction remains anchored within the abdomen,
whereas the greater curvature of the stomach rolls up
into the chest alongside the distal esophagus.
Eventually, most of the stomach can herniate.
 Because the stomach is anchored at the pylorus and
cardia, however, the body of the stomach undergoes a
180 degree organo-axial rotation, resulting in an upside-
down intrathoracic stomach when it is herniated.
 Type III represents a combination of type I and II.
This type is more common than a pure type II and is
characterized by herniation of both the greater
curvature of the stomach and the GE junction into the
chest.
 A type IV HH occurs when abdominal organs other than
or in addition to the stomach herniates through the
hiatus.
Typically, these hernias are large and contain colon or
spleen in addition to the stomach within the chest.
 ANATOMY

Type II Type III Type IV

Ciaran OHare
 Symptoms
Type I: GE reflux associated
Type II, III, and IV: post prandial pain or bloating, early
satiety, breathlessness with meals, and mild dysphagia
related to compression of the distal esophagus by the
adjacent herniated stomach.
The herniated stomach is susceptible to volvulus,
obstruction, and infarction and can develop ischemic
longitudinal ulcers (Cameron Ulcer) with frank
or occult bleeding.
 Diagnosis and Evaluation
Chest X-ray: fluid air level in the posterior mediastinum
on lateral X-ray
Barium swallow: diagnostic
EGD: to see coexisting abnormalities and define location
of GE junction
CT
Management
1. Asymptomatic sliding hernias: no treatment
2. Sliding hernia and GER with mild esophagitis: H2
blockers, PPI
3. Failed medical therapy, young patients or severe
esophagitis: anti-reflux procedure and HH repair
4. Patients with no reflux but have symptoms related to
their hernia (chest pain, intermittent dysphagia, or
esophageal obstruction) should undergo HH repair.
5. All patients with type II, III, or IV HH: surgical repair
GERD
Abnormal exposure of the distal esophagus to
refluxed stomach contents.
In 60% of patients mechanically defective LES is
responsible for the GER.
Sphincter function of the LES depends on the
integrated mechanical effect of the sphincters
intramural pressure and the length of exposed to
intra-abdominal positive pressure.
 Other etiologies: inefficient esophageal clearance
of refluxed material, fixed GOO, functional delayed
gastric emptying, increased gastric acid secretion,
and inappropriate relaxation of the LES.
 Symptoms
Posture dependent substernal or epigastric burning pain
that is relieved by antacids.
Regurgitation, dysphagia and excessive flatulence.
Atypical: mimicking laryngeal, respiratory, cardiac,
biliary, pancreatic, gastric, or duodenal diseases.
 Diagnosis and evaluation
Upper GI contrast study
EGD
Esophageal manometer
Esophageal PH testing
Gastric emptying study
 Mean HPZ pressure less than 6mmHg or overall
length less than 2cm, is more likely to be associated
with incompetence of the LES.
 Treatment
Medical treatment
Remain upright after meal, elevate bed
Dietary alterations
Pharmacologic therapy: anatcid, H2B, PPI, prokinetic
Transoral endoscopic suturing
 Surgical
Laparoscopic, transabdominal approach: Nissen fundoplication,
Hill posterior gastropexy, Toupet fundoplication
Transthoracic approach: Nissen, Belsey Mark IV repair, Collis
gastroplasty
Functional Esophageal Disorders
Motor disorders of the esophageal skeletal muscle
Result in defective swallowing and aspiration
Potential causes can be classified into five: neurogenic,
myogenic, structural, iatrogenic, and mechanical.
Cricopharyngeal myotomy can provide relief
 Motor disorders of esophageal smooth muscle and
LES: primary and secondary
Primary dysmotility: achalasia, vigorous achalasia,
DES, nutcracker esophagus, hypertensive LES
Secondary dysmotility: progressive systemic
sclerosis (scleroderma)
 Achalasia: most common primary esophageal
motility disorder.
Presents between the ages of 35 and 45 years.
Unknown etiology
Characterized by loss of the LES to relax with
swallowing, resulting in esophageal dilatation.
LES pressure is usually elevated.
 Symptoms
Progressive dysphagia
Regurgitation
Odynophagia
Aspiration with resultant bronchitis and pneumonia
Chest pain
 Diagnosis
Chest X-ray: fluid filled, dilated esophagus, and
absence of a gastric air bubble.
Barium esophagogram: tapering (Birds Beak) of the
distal esophagus and dilated proximal esophagus.
Manometer: definitive test (absence of peristalsis,
mirror-image contractions, and limited or absent
relaxation of the LES with swallowing)
 Manometer: definitive test (absence of peristalsis, mirror-
image contractions, and limited or absent relaxation of the
LES with swallowing)
 Medical treatment
Aimed at decreasing LES tone and includes nitrates, CCB,
pneumatic dilatation and endoscopic injection of
botulinium toxin, often provide highly effective therapy.
Beneficial in 10% of patients
 Surgery
Hellers esophagomyotomy: excellent result in 90%-98%
of patients.
A concomitant antireflux procedure with the
esophagomyotomy helps avoid late stricture due to
GERD caused by the incompetent LES.
Esophageal Ca
Epidemiology
Worldwide the total number of new cases of esophageal
cancer was estimated at 500,000.
Squamous Ca accounts for the majority of cases
worldwide
Has high regional variation
 Risk Factors (squamous Ca)
Food additives- Nitroso compounds
Mineral deficiencies- Zn and Molybdenum
Cigarette smoking, alcohol consumption
Long standing achalasia, lye stricture, tylosis, HPV
GERD and BE are risk factors for Adeno Ca
Clinical Manifestation
Dysphagia (>60% circumference involved)
Pain on swallowing dry food
Tracheobronchial tree involvement gives rise to
coughing, choking and aspiration pneumonia.
 Major vessel erosion
Hoarseness of voice
Jaundice, bone pain
Anorexia, weight loss
Investigation
Barium swallow
Upper GI endoscopy
EUS
CT
PET
PET-CT
Treatment
Palliative or curative
Palliation is indicated for advanced cases
Chemoradiation
Stent
Surgery
Trans-Hiatal Esophagectomy
Ivor-Lewis Esophagectomy
McKeown Esophagectomy
Complications
Anastomotic leak
Conduit necrosis
Stricture