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- portal-
systemic 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 enlargement-
hypersplenism
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