Powerpoint: Disorders Of The Esophagus

DISORDERS OF THE ESOPHAGUS

ANATOMY OF THE ESOPHAGUS • Hollow muscular tube guarded by

upper and lower sphincters • Extends from the lower border of the cricoid (C6) to the stomach • The length- 25 to 30 cm. • Viewed endoscopically- 15 cm. from the teeth till 40 cm. at cardioesophageal junction

The middle of the esophagusopen tubular view, pink coloration. Sweeping wave like contractions are what move food

ANATOMY OF THE ESOPHAGUS • Posterior mediastinum • Diaphragmatic hiatus in front of the aorta • Cervical esophagus best approached in the left side of the neck • Middle thoracic esophagus- approached by right thoracotomy • Distal esophagus-approached by left thoracotomy

ANATOMY OF THE ESOPHAGUS • Cardia = gastr-esoph. junction, the

junctional zone between pale squamous esophageal mucosa and pink gastric mucosa, Z line • Up to 3 cm. of gastric mucosa type extending up the esophagus is accepted as normal • More than that indicates Barret’s esophagus

ASSESSMENT OF ESOPHAGEAL DISEASE • Careful history • Physical examination • Appropriate investigations

SYMPTOMS OF ESOPHAGEAL DISEASE • Dysphagia- difficulty in swallowing • May be due to- organic disease (benign

strictures or esophageal carcinoma) - esophagal motility disorders (achalasia or diffuse esophageal spasm) • Dysphagia for solids implies severe disease, organic or functional • Dysphagia for liquids- motility disorders

SYMPTOMS OF ESOPHAGEAL DISEASE • Regurgitation- effortless return of the

gastric content into the mouth • Postural regurgitation is a common symptom in reflux disease • Precipitated by meals and increased in intraabdo.pressure • Overflow regurgitation into the pharynx-trachea- aspiration pneumonitis

SYMPTOMS OF ESOPHAGEAL DISEASE • Odynophagia- painful swallowing- organic

disease- esophagitis • Esophageal pain- two sorts: heartburn and angina-like tightening pain • Heartburn is due to reflux of gastric juice to the esophagus- esophagitis • Angina-like tightening pain-esophageal anterior chest pain, simulates angina pectoris- reflux esophagitis, motility disorders

Atypical Presentation of Esophageal Disease • Anemia due to chronic blood loss- erosive esophagitis • Acute upper GI bleeding- Mallory-Weiss sdr.,peptic ulcer in a hiatus hernia • Severe sepsis, respiratory distressperforation of the esophagus • Angina-like pain- reflux disease • Pulmonary symptoms- aspiration pneumonitis- reflux disease

ESOPHAGEAL DISEASE PHYSICAL SIGNS • Inaccesible to physical examination • Evidence of weight loss • Palor due anemia • Neck swelling • Chest signs • Hepatomegaly

ESOPHAGEAL DISEASE INVESTIGATIONS • CXR, Barium swallow, CT scan • USS, external, endoscopic • Radioisotope studies- labelled bollus • Endoscopy with biopsy, cytology • Manometry • Ph 24-hours monitoring • Tests to exclude cardiac disease- ecg, coronary angiography

ESOPHAGEAL DISEASE INVESTIGATIONS • CXR may reveal: - aspiration pneumonitis, - mediastinal widening, - fluid/gas level, - mediastinal emphysema, - pleural effusion

ESOPHAGEAL DISEASE INVESTIGATIONS • Barium swallow- indications – – – – –

Esophageal motility disorders Esophageal carcinoma and benign stricture Gastro-esophageal reflux +/- hiatus hernia Suspected esophageal perforation Leaking esophageal anastomosis

ESOPHAGEAL DISEASE INVESTIGATIONS • CT scan- preop.assessment of esophageal malignancy - extent of mural invasion, - involvement of adjacent structures, - mediastinal lymph nodes

ESOPHAGEAL DISEASE INVESTIGATIONS • Radioisotope studies- assess g-e

incompetence: - in pts. with reflux symptoms - esophageal transit of liquid and solid boluses in pts. with motility disorders

ESOPHAGEAL DISORDER INVESTIGATIONS • Endoscopy- essential in all pts.with dysphagia

– visual information- severity of esophagitis – esophageal cancer- biopsy, cytology – gastro-esophageal reflux

ESOPHAGEAL DISEASE INVESTIGATIONS • Physiological tests – manometry- the pressure profilemotility disorders – 24h.pH monitoring- pathological reflux is considered when the time in the acid zone Ph<4 is more than 5 min.

ESOPHAGEAL MOTILITY DISORDERS • Cricopharyngeal dysfunction • Achalasia • Diffuse esophgeal spasm

CRICOPHARYNGEAL DISFUNCTION • Failure of the UES to relax properly • Pharyngoesofageal diverticulum- Zenker’s • False diverticulum- mucosa herniates posteriorly between the fb.of CPH.muscle • Frequently associated with hiatus hernia and GER. • Symptoms: dysphagia, mass in the neck, tracheal compression

CRICOPHARYNGEAL DYSFUNCTION • Diagnosis: – – – –

history physical examination barium swollow endoscopy

CRICOPHARYNGEAL DYSFUNCTION

• Treatment: – Cricopharyngeal myotomy – Excision of the diverticulum+myotomy

Formation of pharyngoesophageal (Zenker's) diverticulum. Left- herniation of the pharyngeal mucosa and submucosa occurs at the point of transition (arrow) between the oblique fibers of the thyropharyngeus muscle and more horizontal fibers of the cricopharyngeus muscle (Killian's triangle). Center and right— as the diverticulum enlarges, it dissects toward the left side and downward in the superior mediastinum in the prevertebral space.

Barium swallow- Zenker’s diverticulum

ACHALASIA • Unknown etiology • Abnormal peristalsis in the body of the esophagus, resulting in:

– high resting LES pressure – failure of the LES to relax during swollowing

The body of the esophagus becomes dilated Carcinoma of the esophagus is 10 times commoner in pts. with achalasia

ACHALASIA • Symptoms: – – – – –

Difficulty in swollowing fluids Respiratory symptoms Vomiting Retrosternal pain Weight loss

ACHALASIA • Diagnosis:-contrast studies- smooth

tapering narrowing of lower esoph. end with dilated, tortuous lower esophagus, uncoordinated or absent peristalsis • Esophageal manometry • Esophagoscopy

ACHALASIA • Treatment: – Non surgical treatment- pneumatic dilatation of the LES – Surgical- esophagomyotomy (Heller’s op.) • Myotomy is confined to the lower portion of the esophagus, 7-10 cm. and upper gastric muscle • Esophagomyotomy can be combined with an antireflux procedure

TREATMENT • As the degenerative neural lesion of this

disease cannot be corrected, treatment is directed at palliation of symptoms and prevention of complications.

• Effective peristalsis is rarely restored by

successful treatment, but improved oesophageal emptying and a decrease in oesophageal diameter are generally expected.

Pharmacotherapy : • Smooth muscle relaxants alleviate symptoms and •

improve oesophageal emptying in up to 70% of patients. Nitrites, such as sublingual isosorbide dinitrite, and calcium channel blockers, such as diltiazem, nifedipine and verapamil, have this effect.

• This treatment option is suitable for patients with medical conditions that interfere with pneumatic dilatation or myotomy.

Botulinum Toxin: • Botulinum toxin type A is derived from the controlled

fermentation of Clostridium botulinum. • The toxin binds to presynaptic cholinergic neuronal receptors, interferes with acetylcholine release. • Botulinum toxin decreases LOS basal tone and improves symptoms in patients with achalasia. • Beneficial response occurs in 90% of patients, but symptoms reappear within a year in many initial responders.

Dilatation: • Forceful dilatation of the gastroesophageal sphincter to a • • • • •

diameter of 3 cm is necessary to tear the circular muscle and to ensure a lasting reduction in LOS pressure. Pneumatic dilators are conventionally used today. Water-soluble contrast material is used to detect distal oesophageal leaks. Surgical consultation is undertaken if perforation is evident. Small perforations are managed conservatively with broadspectrum antibiotics. Clinical deterioration e.g. shock, sepsis, haemorrhage or a finding of free-flowing barium into the mediastinum, requires immediate thoracotomy and repair.

Dilatation • At least 60% of patients have a good response • The response rate varies with patient age, (younger

patients do not do as well as older patients), and duration of symptoms, (those with a shorter history do not respond as well)

• Morbidity is mostly related to oesophageal perforation, a complication in approximately 5% of patients, but surgical repair is required in less than half of these cases.

Surgery: • The Heller procedure was described in

1913 and now a modification of this procedure is used most commonly in the surgical management of achalasia

• An anterior myotomy is performed by dividing the circular muscle of the oesophagus down to the level of the mucosa.

Minimally invasive surgical procedures • A preferable alternative to open myotomy, allowing the Heller

myotomy to be performed thoracoscopically and laparoscopically

• Shorter hospitalisation, less pain and early resumption of activity

are the benefits of the minimally invasive approach, which remains as effective as the open techniques in the relief of dysphagia.

• Complications of minimally invasive surgery include: anterior

gastric perforation, mucosal perforation at the gastroesophageal (GO) junction and, most significantly, GOR

Comparisons between therapies • Pneumatic dilatation, pharmacotherapy and botulinum

toxin injection are easy to use, usually well-tolerated and relatively cheap treatment options in achalasia. • Surgery generally gives longer-lasting results as well as more complete relief of symptoms. • Non-operative therapy is recommended initially. Patients are only referred for surgery if they remain symptomatic after 3 attempts at pneumatic dilatation.

a: Initial esophagram of patient with early achalasia and no esophageal dilation. b: Patient after 2 years of nonoperative treatment. Note significant esophageal dilation and air-fluid level compared to pretreatment. c: End-stage achalasia with sigmoid or megaesophagus.

After satisfactory cardioesophageal myotomy, a Toupet fundoplication is done- the posterior fundus of the stomach is brought around the esophagus and secured to the right crus and the right cut edge of the myotomy. In a similar (in fact mirror image) fashion the anterior fundus is sutured to the left crus and left edge of the myotomy.

DIFFUSE ESOPHAGEAL SPASM • Strong nonperistaltic contractions • Normal sphincter relaxation • May be associated with GER • Symptoms: chest pain • Manometry-high amplitute repetitive contractions • Constrast study: normal in ½, segmental spasm, diverticula

DIFFUSE ESOPHAGEAL SPASM • Treatment: – Surgery- long esophagomyotomy, from the arch of the aorta to just above the LES,-antireflux op in case of GER – Medical treatment- calcium channel blockers and smooth muscle relaxants

GASTRO-ESOPHAGEAL REFLUX • Secondary to LES dysfunction • LES dysfunction may be related to: – –

Decreased gastrin production Operation on or near the esophageal hiatus – Sliding hiatus hernia – Scleroderma – Tabacco and alcohol

GASTRO-ESOPHAGEAL REFLUX • Diagnosis: • Substernal pain, heartburn,

regurgitation • Manometry-decreased LES pressure • Esopgagoscopy-esophagitis • 24h pH monitoring • Cineradiography

GERD-when acid from the stomach bathes the lower esoph. A feeling of heartburn occurs.This can cause some mild inflammation.

GERD- lower esoph. with a slight erosion surrounded by inflammed red tissueesophagitis gr.II

GERD- extensive deep ulceration, severe case of esophagitis (gr.III)

GERD- severe case of extensive deep ulcerations in the lower esoph

GASTRO-ESOPHAGEAL REFLUX • Treatment – Medical: antiacids and metoclopramide – Surgical: antireflux operations- Nissen fundoplication- wrapping the lower esophagus with gastric fundus Indications for surgery: -sy.refractory to medical treatment -severe esophagitis, Barret’s esophagus (replacement with columnar epithelium in the lower esophagus secondry to esophagitis)

Barrett’s occurs after longstanding reflux of acid. The stomach lining grows up where does not belong. Red stomach tissue creeping up

Barrett’s- significant progression

Barrett’s- extensive long fingers and patches of Barrett’s- prone to malignant changes

BARRETT’S ESOPHAGUS • Replacement of the lower esophagus with

gastric-type mucosa, exceeding 3 cm. above the squamo-columnar junction and gastric mucosa islands amongst the squamous mucosa • Recognized as a metaplastic response to reflux with increased exposure to gastric acid • 30-fold increased risk of developing an adenocarcinoma • Regular endoscopic surveillance until an early adenocarcinoma is detected