Powerpoint: Disorders Of The Esophagus Ii

HIATAL HERNIA

HIATAL HERNIA Distal esophagus- held in position by the

phrenoesophageal ligament Occurs most commonly in women Most hiatal hernias are asymptomatic 5-10% of pts.will develop GERD There is strong association with obesity Saint’s triad= gall stones+colonic diverticular disease+hiatal hernia

HIATAL HERNIA Type I or sliding HH: ph.-esoph.lig.intact but

lax- distal esoph. and cardia herniate through the hiatus. Type II or paraesophageal HH- focal defect of the ph.-esoph. lig.,greater curvature herniates upward alongside the esoph. Type III- a combination of type I and II

HIATAL HERNIA SYMPTOMS Type I- sy.of associated GERD Type II, III- postprandial pain,

- bloating, - breathlessness with meals, - mild dysphagia The herniated gastric pouch is susceptible to volvulus, obstruction, infarction, ischemic ulcers, occult bleeding, perforation, gangrene.

HIATAL HERNIA DIAGNOSIS AND EVALUATION CXR- air/fluid level in post.M.on lat.view Barium swallow- the dg.study of choice Esophagoscopy- for GERD and esophagitis Manometry and pH testing for refux sy.

Hiatus hernia seen from below with the endoscope in an inverted position inside the stomach

HIATAL HERNIA MANAGEMENT Asymptomatic HH- no treatment HH+GERD- medical treatment Indications for surgery: Symptomatic HH (chest pain, dysphagia) HH+ severe esophagitis HH type II, III

Oprative objectives: - reduction of hernia - closure of the hiatal defect - antireflux procedure

ESOPHAGEAL STRICTURES Caustic stricture Strictures secondary to reflux esophagitis

CAUSTIC STRICTURES Caused by ingestion of caustic agents: lye,

soda, acids Commonly taken: caustic soda, sulphuric acid from car batteries in attempted suicide Diagnosis: - history of caustic ingestion - sy: retrosternal pain, dysphagia, shock - endoscopy- the severity and extent of lesions

CAUSTIC LESIONS Pharynx is relatively spared- short contact time Edema of the laryngopharynx- respiratory sy. Esoph. takes the brunt of the injury- inflammation,

ulceration, necrosis, perforation Stomach is protected- its contents dilute whatever and neutralizes alkali. Perforation can occur between 3h.-3 weeks Early endoscopy within a few hours of injury is the key Complete endoscopy should not be attempted if there is a severe necrotizing lesion and air insuflation is kept to a minimum

CAUSTIC STRICTURES Treatment:

- fluid ressuscitation, - total parenteral nutrition, - antibiotics, - steroids Barium swollow after 10-14 days Strictures- dilatation treatment 3/4w.after injestion or esophageal replacement

SECONDARY STRICTURES Caused by acid GERD with mucosal

destruction and subsequent healing Common site- GE junction Diagnosis- history of reflux sy.+ dysphagia Barium swollow confirms the dg. Endoscopy- extent of lesion, rule out a ca. Treatment- dilatation+ antireflux op - reconstructive procedure

TUMORS OF THE ESOPHAGUS Benign lesions- < 1% of all neoplasms The commonest is leiomyoma Occurs in the lower esoph.as uniform, oval

swelling, protruding into the lumen, covered by intact mucosa Main symptom- dysphagia Well incapsulated- removal by enucleation

ESOPHAGEAL CANCER Mostly are carcinomas- bad prognosis The predominant histo.type is squamous Premalignant conditions: acalasia, esophagitis

and Barret’s esophagus Macroscopically- 3 forms: polypoid, stenosing and ulcerative Surgical treatment for early ca.-5-years survival of 80-85%

SQUAMOUS-CELL CARCINOMA Infiltrates the submucosal plane,

longitudinally and circumferentially Invades the muscle walls and adjacent mediastinal structures Common in the middle and lower third Lymph node spread: cervical, mediastinal, subdiaphragmatic Metastatic spread to the liver and bones Sensitive to radiotherapy

Endoscopic view of the esophageal squamous cell carcinoma

ADENOCARCINOMA OF THE ESOPHAGUS Originates from Barret’s epithelium, following

longstanding GERD Common in the lower third Prognosis is poor Insensitive to radiotherapy Mode of spread similar to that of squamous tumors

Protruding esophageal carcinoma

ESOPHAGEAL CANCER DIAGNOSIS Symptoms: dysphagia, weight loss, pain Investigations: barium swollow and endoscopy

with biopsy Lesions longer than 5 cm.usually unresectable Investigations for staging: laryngoscopy, diaphragmatic USS, bronchoscopy, CT/MRI, laparoscopy

Adenocarcinoma of the esophagus at 35 cm. distance from the incisors, invasion of the aorta

Eso-tracheal fistula typical for squamous cell carcinoma

ESOPHAGEAL CANCER TREATMENT Surgical excision By-pass operation Radiotherapy Chemotherapy Laser coagulation Transtumoral intubation Feeding gastrostomy/jejunostomy

PERFORATION OF THE ESOPHAGUS Intraluminal causes: - instrumental injuries during endoscopy,

dilatations, tube passage,

- foreign bodies, -

caustic substance injestion, cancer of the esophagus, barotrauma (Boerhaave’s syndrome)

PERFORATIONS OF THE ESOPHAGUS Extraluminal causes: - penetrating injuries: stab wounds, gunshot

wounds - blunt trauma due to rapid increase in intraluminal pressure - operative injuries: thyroid resection, anterior cervical spine operations, vagotomy, laparoscopic fundoplication

PERFORATION OF THE ESOPHAGUS Symptoms and signs: - dysphagia, - chest pain, - fever, chills - leukocytosis, - tachycardia, - respiratory distress and septic shock

PERFORATION OF THE ESOPHAGUS Cervical perforation: - neck stiffness, - subcutaneous emphysema Intrathoracic perforation: - chest pain, - subcutaneous emphysema, - dyspnea, - pleural effusion

ESOPHAGEAL PERFORATION DIAGNOSIS History Physical examination: - crepitation in the neck, - crunching sound over the heart (Hamman’s

sign), - breath sounds diminished (pleural effusion) Investigations: - CXR: air in the M.,pneumothorax,pleural effusion - esophagography

Esophageal perforation

ESOPHAGEAL PERFORATION TREATMENT Controversy- non-op.and op.management Nil by mouth, 5 days Broad spectrum antibiotics Antiacid drugs Pleural drainage Mediastinal collection- surgery for drainage

and esophageal divertion

MALLORY-WEISS SYNDROME Presents as acute upper GI bleeding Partial thickness tear near the GE junction Follows a prolonged period of severe vomiting

and retching Diagnosis is made by endoscopy Treatment: conservative as in most cases bleeding subsides spontaneously

ESOPHAGEAL VARICES Result from portal venous hypertension The most common cause is cirrhosis usually

associated with alcohol abuse Abnormal venous communications develop between the peripheral part of the portal system and the systematic circulation- portalsystemic shunting

ESOPHAGEAL VARICES Large veins appear at the lower end of the

esophagus and gastric fundus These varices are easily traumatised by food and produce massive GI bleeding Up to 40% of cirrhotic patients suffer variceal hemorrhage at some stage A further result is splenic enlargementhypersplenism Portal-systemic encephalopathy- ammonia

ESOPHAGEAL VARICES MANAGEMENT Elective injection sclerotherapy Acute bleeding- resuscitation

- balloon tamponade Surgery-less commonly performed - transgastric esophageal stapling The best treatment- repeated injection sclerotherapy