DISEASES OF

ESOPHAGUS

DR. MUKESH SHARMA

DEPT OF SHALYA TANTRA
• ESOPHAGUS ANATOMY
❖The esophagus is a fibromuscular tube, approximately 25 cm in
length that transports food from the pharynx to the stomach.
❖ It originates at the inferior border of the cricoid cartilage (c6),
extending to the cardiac orifice of the stomach (T11).
❖The esophagus originates in the neck, at the level of the sixth
cervical vertebrae. It is continuous with the laryngeal part of the
pharynx.
❖It descends downward into the superior mediastinum of the thorax. Here,
it is situated between the trachea and the vertebral bodies T₁ to T4 .
❖It then enters the abdomen by piercing the muscular right crus of the
diaphragm, through the oesophageal hiatus (simply, a hole in the
diaphragm) at the T10 level.
❖The phreno-oesophageal ligament connects the oesophagus to the border
of the oesophageal hiatus. This permits independent movement of the
oesophagus and diaphragm during respiration and swallowing.
❖The abdominal part of oesophagus is approximately 2 cm long, it
terminates by joining the cardiac orifice of the stomach at level of T11.
CONGENITAL
ANOMALIES
TRACHEO – ESOPHAGEAL FISTULA ( TE FISTULA )
This is the most common congenital anomalies of oesophagus.
• This condition is often associated with hydramnios, so in all cases of hydramnios
possibility of TE fistula is considered.
• It may be associated with VACTER anomalies.
V: Vertebral defects
A: anal atresia.
C: Cardiac defect (PDA/VSD)
TE: Tracheo-esophageal fistula
R: Radial hypoplasia and renal agenesis
TYPES
• There are four types of tracheo–esophageal fistula:
❖Type 1: It accounts 85% of all tracheo–esophageal fistula, in which upper esophageal
segment ends blindly and lower portion of the esophagus is connected with the trachea
through tracheo-esophageal fistula.
❖Type 2: It accounts 8% to 10% of TE fistula, in which both upper and lower
esophageal segments end blindly with a portion of esophagus in between missing.
❖Type 3: It accounts 1 -2% of TE fistula, in which upper segment is connected with TE
fistula and lower segment ends blindly.
❖Type 4: It accounts less than 1% of TE fistula, in which both upper and lower
esophageal segments are connected with trachea through TE fistula.
• CLINICAL FEATURES
❖TE fistula should be recognized within 24 hours of birth.
❖Newborn baby regurgitates all feeds and there is continuous
pouring of saliva from the mouth which is a diagnostic feature.
❖Cough, cyanosis and respiratory distress.
❖It is commonly associated with maternal hydramnios (50%).
INVESTIGATIONS
❖Obstruction is revealed while passing naso-gastric tube.
❖Contrast study reveal fistula and obstruction (Dionosil
1ml is used for contrast medium).
❖Chest X-ray to see trachea.
❖Echocardiography.
MANAGEMENT
• Management is surgical correction of fistula. The
tracheoesophageal fistula is divided in ligatures and end to
end anastomosis is per formed between proximal and distal
segment of esophagus.
• This provide satisfactory outcome nearby normal esophagus
functions in most of the patients.
REFLUX
ESOPHAGITIS
• Reflux of small amounts of gastric juice into the oesophagus is a normal
physiologic event.
• Reflux esophagitis occurs when this reflux becomes excessive.
• Normal competence of the gastro-esophageal junction is maintained by the
LES (lower esophageal sphincter). This is influenced by both its
physiological function and its anatomical location relative to the diaphragm
and the oesophageal hiatus.
• In normal circumstances, the LES transiently relaxes during swallowing,
burping, belching and allows vomiting to occur and in response to stretching
of the gastric fundus, particularly after a meal to allow swallowed air to be
escaped.
• Most episodes of physiological reflux occur during postprandial phase due
to transient lower esophageal sphincter relaxations.
TYPES
• Acute: Following burns, trauma, infection, peptic
ulcer.
• Chronic: Reflux of acid in sliding hernia or after
gastric surgery.
ETIOLOGY
❖Sliding hernia usually associated with GERD.
❖Systemic collagen diseases like scleroderma involving oesophagus may cause reflux
esophagitis. In these cases there is loss of oesophageal sphincter tone and paralysis of
oesophageal muscle that cause GERD.
❖Delayed gastric emptying causes GERD.
❖Reduced incidence of peptic ulcer as the incidence of infection with Helicobacter pylori
as a result of improved socioeconomic conditions along with a rising incidence of
GERD in the last 20-30 years. The cause of the increase is unclear, but may be due to
increasing obesity. The strong association between GERD, obesity and the parallel rise
in the incidence of adenocarcinoma of the oesophagus represents a major health
challenge.
PATHOLOGY
There is bleeding granulation tissue in lower esophageal mucosa with spasm of
longitudinal muscle which pulls the adjacent gastric area and following fibrosis.
• Grading
Grade 1: Mucosal erythema
Grade 2: Mucosal erythema + superficial ulceration
Grade 3: Mucosal erythema + superficial Ulceration + submucosal fibrosis
Grade 4: Mucosal erythema + extensive Ulceration + para mural fibrosis
 CLINICAL FEATURES
❖It is a sequel of GERD (Gastro-esophageal reflux disease).
❖Pain and burning sensation in retrosternal area often referred to shoulder, neck
and arm. Sometimes it mimics angina pectoris. Pain increases on lying down.
❖Heart burn is common.
❖Dysphagia due to muscle spasm and edema (inflammation) or due to fibrotic
stricture.
❖Anemia due to hemorrhage from esophageal ulcer.
 INVESTIGATIONS
• Barium meal – It may reveal hiatus hernia.
• Esophagoscopy and biopsy – It reveals
inflammation and ulcerations.
 MANAGEMENT
Conservative management
❖ The patient should be advised to sleep with elevated head end of the bed.
❖ Not to eat just before bed time.
❖ Smoking, alcohol, excessive consumption of tea and coffee should be avoided.
❖ Patient should be advised to reduce weight. Tight fitting garments that increases intra abdominal pressure,
should be avoided.
❖ Antacids should be taken one hour after meal and before bed time.
❖ H₂ blockers: Ranitidine, famotidine.
❖Proton pump inhibitors: More effective drugs. Omeprazole 20 mg BD one hour before food (Morning)
for 6 months, Lansoprazole 30 mg, Pantoprazole 40 mg, Rabeprazole 20 mg (can be given with food).
❖Prokinetic drugs like metochlopramide, domperidone, cisapride, mosapride
Surgical management
The indications of surgery are:-
❖When conservative management fails.
❖Recurrence of disease.
❖Ulceration and stricture formation.
❖Severe dysphagia.
❖Surgical operations are Nissen fundoplication, Belsey mark iv operation,
Hill procedure, in these operations the lower esophageal sphincter is repaired and
abdominal esophagus is narrowed.
❖Resection has to be performed in severe cases.
ESOPHAGEAL
VARICES
❖Esophageal varices are abnormal, enlarged veins in the lower part of the
esophagus. This condition occurs most often in person with serious liver
diseases.
❖Esophageal varices are Porto-systemic collaterals – i.e., vascular channels
that link the portal venous and the systemic venous circulation.
❖These occurred as a consequence of portal hypertension (a progressive
complication of cirrhosis), preferentially in the sub mucosa of the lower
esophagus.
❖Rupture and bleeding from esophageal varices are major complications of
portal hypertension and are associated with a high mortality rate.
❖Variceal bleeding accounts for 10-30% of all cases of upper gastrointestinal
bleeding.
 ETIOLOGY
• Esophageal varices form when blood flow to the liver is blocked,
most often by scar tissue in the liver caused by liver disease. The
blood flow begins to back up, increasing pressure within the large
vein (portal vein) that carries blood to the liver.
• This pressure (portal hypertension) forces the blood to escape
other pathways through smaller veins, such as those in the lowest
part of the esophagus. These are thin-walled enlarged veins (like
balloon filled with blood). Sometimes the veins can rupture and
bleed.
Causes of esophageal varices include:
• Severe liver scarring (cirrhosis): A number of liver diseases including hepatitis infection,
alcoholic liver disease, fatty liver disease and a bile duct disorder called primary biliary
cirrhosis can result in cirrhosis.
• Blood clot (thrombosis): A blood clot in the portal vein or in a vein that feeds into the
portal vein (splenic vein) can cause esophageal varices.
• Parasitic infection: Schistosomiasis is a parasitic infection found in parts of Africa, South
America, the Caribbean, the Middle East and Southeast Asia. The parasite can damage the
liver, as well as the lungs, intestine and bladder.
• A syndrome that causes blood back to the liver – Budd-Chiari syndrome is a rare
condition that causes blood clots that can block the veins that carry blood out of the liver.
 SYMPTOMS
❖Esophageal varices usually don’t cause signs and symptoms unless they bleed.
Signs and symptoms of bleeding esophageal varices include:
❖Hematemesis (Blood in vomit),
❖Black, tarry or bloody stools,
❖Lightheadedness,
❖Loss of consciousness (in severe case)
❖Signs of liver disease like jaundice, ascites, pruritus etc.
 COMPLICATIONS
• The most serious complication of esophageal varices is bleeding.
• Once a patient have had a bleeding episode, the risk of another
episode is greatly increased.
• In some cases, bleeding can cause the loss of so much blood
volume that may cause shock and even death.
INVESTIGATIONS
• Blood test,
• Liver function tests,
• Endoscopy to visualize esophageal varices,
• USG abdomen,
• Liver angiography to measure portal pressure and to visualize abnormal venous anatomy
of liver,
• Measurement of portal venous pressure : This can be performed by direct measurement
through transhepatic portography, umbilical vein and splenoportography.
MANAGEMENT
When there is acute variceal bleeding the management is performed in three stages
❖Resuscitation
• Blood volume should be maintained by blood transfusion.
• Pulse rate, B.P., urine output should be monitored.
• Sedation.
• Inj. Vit. K in case of defective coagulopathy.
❖Specific measures
• Treatment of esophageal varices.
• By vasopressin (vasoconstrictor)
• Using elastic bands to tie off bleeding veins: During variceal ligation, the varices are tied
off with an elastic band, so they can’t bleed. Variceal ligation carries a small risk of
complications, such as scarring of the esophagus.
• By injection of sclerosant solution in varices.
• Balloon tamponade: This is a temporary method to control acute bleeding from
esophaseal varices. Sangstaken – Blakemore tube is usually used. It is inflated with
300ml of air and appropriate pressure is applied on varices.
❖Measures to reduce portal pressure
• Drugs to reduce the portal pressure like propranolol, nadolol, isosorbide-5-mono nitrate.
• Surgeries: Portosystemic shunt operation.
• TIPSS (Transjugular intrahepatic porto systemic stent shunts): It is used if all other
earlier methods mentioned have failed. It commonly controls the un controlled acute
bleeding and prevents further bleed and also acts as a bridge for future transplantation.
The portal pressure is reduced by transfer the pressure to systemic circulation by stent
(connection between portal and systemic circulation).
• Liver transplantation: Liver transplant is becoming popular for cirrhosis with varices.
It is ideal, final and best, but donor availability and cost is the problem.
ESOPHAGEAL
ULCER
 BARRETT’S ULCER OR BARRETT’S ESOPHAGUS
• It is an ulcer in columnar epithelium lined Barrett’s esophagus (It is the
metaplastic changes in the mucosa of the esophagus as the result of GERD.
Squamous epithelium of lower end of the esophagus is replaced by columnar
epithelium.) at or just above the squamocolumnar junction.
• It causes:
Bleeding.
Perforation.
Adenocarcinoma of esophagus.
• TREATMENT for Barrett’s ulcer is endoscopic biopsy and resection.
MALLORY-WEISS SYNDROME
• It is seen in adults with severe prolonged vomiting, causing
longitudinal tear in the mucosa of esophagus and stomach at and
just below the cardia, and leading to severe hematemesis.
• Violent vomiting often may be due to migraine or vertigo or
following a spell of alcohol.
• It presents with severe vomiting and later hematemesis, with
features of shock.
TREATMENT
• General conservative, if it is only a mucosal tear.
• Blood transfusion.
• Sedation.
• Hemostatic agents like vasopressin.
• Surgery is required when bleeding is continuous.
TUMOURS OF THE
ESOPHAGUS
Tumours of the esophagus could be classified in two categories:
• Benign tumours
• Malignant tumours
BENIGN TUMOURS
Benign tumours of the esophagus are rare and constitute only 1% to 5% of esophageal
neoplasms.
LEIOMYOMA
• This is the most common benign tumour. It is found in patients between 20 and 50 years of
age. Majority of this tumour occur in the middle and lower third of the esophagus.
Histologically, this tumour consists of bundles of smooth muscles.
LEIOMYOMA
• This is the most common benign tumour. It is found in patients between
20 and 50 years of age. Majority of this tumour occur in the middle and
lower third of the esophagus. Histologically, this tumour consists of
bundles of smooth muscles.
CLINICAL FEATURES
➢This tumour may give rise to symptoms only when it is more than
5cm in diameter.
➢The symptoms are dysphagia and vague retrosternal pain.
➢Bleeding may occur when there is malignant transformation to
leiomyosarcoma.
➢Multiple leiomyomas are known as leiomyomatosis.
INVESTIGATIONS
• Barium esophagogram usually diagnoses this condition.
• Esophagoscopy is indicated to rule out malignant lesions. Biopsy taking through
esophagoscopy is not advised as scarring may cause subsequent resection difficult.
TREATMENT
• Excision of the tumour : Even asymptomatic leiomyomas should be excised, as
ultimately they grow larger and definitely cause symptoms. Further, malignancy can
only be ruled out by excisional biopsy.
MALIGNANT TUMOUR
CARCINOMA OF THE ESOPHAGUS
• It accounts less than 1% of all carcinoma and accounts for 7% of all gastrointestinal
Malignancies.
• It is a disease of mid to late adulthood, with a poor survival rate. Only 5-10% of those
diagnosed survive for 5 years.
• Carcinoma esophagus is common in China, South Africa and Asian countries.
• It is less common in America and European Countries.
• In India, it is common in Karnataka and Orissa.
ETIOLOGY
• Age and Gender: Esophageal cancer is predominantly a disease of the old, though it may
occur in young individuals. The usual victims are between 45 to 75 years with highest
incidence between 65 to 75 years. Except the cervical esophagus, where men and women
are equally affected, in thoracic and abdominal esophagus men are more often affected.
• Geographical distribution: The incidence of esophageal cancer is more common from the
shores of Caspian Sea (in north ern Iran) to China, where the incidence is approximately
100 cases per 1 lac of population per annum. The cause of such high incidence in these
areas is not yet known, but is probably due to fungal contamination of food with the
production of a carcinogenic mycotoxin, together with nutritional deficiency in the
population of this area. Supplementation of diet with beta carotene, vitamin E and
selenium has been shown to reduce the incidence of cancer.
• Alcohol and tobacco consumption: These have been thought to increase the incidence of
this disease.
• Malnutrition, vitamin deficiency, anemia, poor oral hygiene also increase the incidence
of esophageal carcinoma.
• Plummer Vinson syndrome: This is a condition of females of over 40 years of age,
characterized by dysphagia associated with iron deficiency anemia. This is a
precancerous condition and increased incidence of carcinoma in cervical esophagus in
women.
• Barrett’s esophagus : It is the metaplastic changes in the mucosa of the esophagus as the
result of GERD. Squamous epithelium of lower end of the esophagus is replaced by
columnar epithelium (columnar metaplasia). It is a premalignant condition and frequently
convert into adenocarcinoma.
• Achalasia cardia (Cardiospasm): It is failure of relaxation of cardia (esophagogastric
junction) due to disorganized esophageal peristalsis causing functional obstruction. A direct
relation has been seen between achalasia and cancer of esophagus. Chance is 10 times
more in patients with achalasia than normal individuals.
• Other esophageal lesions: Hiatus hernia and Reflux esophagitis, corrosive
esophagitis,Esophageal diverticulum etc.
• Incidence of carcinoma of esophagus is
➢Middle third of esophagus: 50%.
➢Lower third of esophagus : 33%.
➢Upper third of esophagus:17%.
SPREAD OF THE TUMOUR
• Direct spread: Lack of serosal layer in esophagus favors local extension. In upper third it
spreads through muscular layer recurrent laryngeal nerve (causes hoarseness), aorta or its
branches (causes fatal hemorrhage, but rare).
• It may perforate and may spread to pleura also.
• Lymphatic spread: Above in the neck, it spreads to supraclavicular lymph nodes. In
thorax, it spreads to paraesophageal, tracheobronchial lymph nodes to sub diaphragmatic
lymph nodes. In abdomen, it spreads to coeliac lymph nodes.
• Blood spread: Spread to liver, lungs, brain and bones.
CLINICAL FEATURES
• Progressive dysphagia is the commonest feature.
• Regurgitation.
• Anorexia and loss of weight (severe), cachexia.
• Pain-sub sternal or in the abdomen.
• Liver secondaries, ascites.
• Bronchopneumonia, melena. Left supraclavicular lymph nodes may be palpable.
• Hoarseness of voice due to involvement of recurrent laryngeal nerve.
• Hiccough, due to phrenic nerve involvement.
 INVESTIGATIONS
• Barium study: Shows irregular rat tail fil ling defect.
• Esophagoscopy: To see the lesion, extent and type.
• Biopsy: For histological type and confirmation.
• Chest X-ray: To look for aspiration pneumonia and metastasis to
lungs.
• Esophageal ultrasonography (EUS): To look for the involvement
of layers of esophagus, nodes, cardia and left lobe of the liver.
• CT scan (95% accuracy).
 MANAGEMENT
• Surgery: Excision of the growth and end to end anastomosis, if metastasis is not
occurred. Sometimes total thoracic and abdominal esophagus is excised
(esophagectomy) and jejunal segment is used to fill the gap between cervical
esophagus and stomach.
• Radiotherapy.
• Chemotherapy.
• SEMS (Self expanding metal stents): To relieve malignant dysphagia