esophagus & diaphragmatic hernia

ESOPHAGUS &DIAPHRAGMATIC HERNIAS

Department of Surgery

HISTOLOGY OF ESOPHAGUS1.Mucosa -Squamous -Changes to columnar epithelium at GE junction2. Submucosa -Contains glands, arteries, -Meissner's neural plexus, lymphatics, veins3. Muscularis -2 layers: outer longitudinal and inner circular4. No serosa -Contributes to increased potential for anastomotic leaks -Contributes to early mediastinal invasion by cancer

ANATOMY OF ESOPHAGUS• The esophagus is a hollow muscular tube approximately 25 cm in

length.

• When the head is in normal position, transition from pharynx to esophagus occurs at lower border of 6th cervical vertebra ---this corresponds to cricoid cartilage anteriorly andpalpable transverse process of 6th cervical vertebra laterally.

• The esophagus is divided into 3 parts: 1. Cervical (approx. 5 cm long) 2. Thoracic (approx. 20 cm long) 3. Abdominal (approx. 2 cm long)

ANATOMY OF ESOPHAGUS

• Cervical esophagus–midline structure positionedposterior and slightly to theleft of the trachea;– approximately 5 cm long– From the level of 6thcervical vertebra to the levelof the suprasternal notchanteriorly– From the level of 6thcervical vertebra to the levelof interspace bet 1st and2nd thoracic vertebraeposteriorly

THORACIC ESOPHAGUS• The thoracic esophagus– In upper portion of thorax itis in intimate relationshipwith the posterior wall oftrachea– Just above the trachealbifurcation, the esophaguspasses to the right of theaorta -- Causes a notchindentation in its left lateralwall– approx. 20 cm long– starts at the thoracic inlet

ABDOMINAL ESOPHAGUS

Abdominal esophagus– attaches to the cardia (or EG junction) of thestomach (is of variable length)

The esophagus has 3 distinctareas of naturally occurringanatomic narrowings:

• Cervical constriction– At the cricopharyngeussphincter (normally closed)– At 15 cm from incisor Teeth

• Bronchoaortic constriction– At the level of aortic arch at 25 cm

• Diaphragmatic constriction– At the level where a physiological sphincter is sited (LES)

• Muscular tube – Conduit from the pharynx tothe stomach

• Passes behind aortic arch and left main bronchus.

• Enters abdomen through esophageal hiatus → 2-4 cm below the diaphragm

• The esophagus has both sympathetic and parasympathetic innervation• The esophagus has an extensive lymphatic drainage that consists of two lymphatic plexuses• Held in position by:– Reflection of the peritoneum onto the stomach– Phreno-esophageal ligament to the oesophagus

ESOPHAGUSESOPHAGUS MUSCLE ARTERY VEIN LYMPH

UPPER STRIATED INFERIOR THYROID

INFERIOR THYROID

DEEP CERVICAL

MIDDLE STRIATED AND SMOOTH

AORTIC AND BRONCHIAL

AZYGOS MEDIASTINAL

LOWER SMOOTH LEFT GASTRIC; INFERIOR PHRENIC

LEFT GASTRIC, CORONARY VEIN

GASTRIC

PHYSIOLOGY OF SWALLOWING

Divided into 3 stages:• Oral Phase (voluntary)• Pharyngeal Phase (involuntary)• Esophageal Phase(involuntary)

ORAL PHASE

• Consists of:– Bolus selection– Preparation– Control– Delivery• Voluntary• Is interrupted or repeated as required for• effective swallow performance

PHARYNGEAL PHASE

• Involuntary• Begins with the passage of bolus into the faucial pillars and ends when the bolus passes the cricopharyngeal segment at the pharyngoesophageal junction

Pharyngeal Phase of Swallowing

1. Elevation of tongue2. Posterior• movement of• tongue3. Elevation of hyoid4. Elevation of larynx5. Tilting of epiglottis

ESOPHAGEAL PHASE

• Involuntary• Consists of coordinated peristalsis• Begins at the UES and ends at the LES

Physiology of the Esophagus

• Its basic function is to transport swallowed material from the pharynx into the stomach• Retrograde flow of gastric contents into the esophagus is prevented by the lower esophageal sphincter (LES)• Entry of air into the esophagus is prevented by

the upper esophageal sphincter (UES)

• Esophageal peristaltic pressures range from 20-100mm Hg with a duration of contraction between 2-4 seconds

• Esophageal contractions-three types:– Primary peristalsis–Secondary peristalsis– Tertiary contractions

Peristalsis• Primary Peristalsis– Initiated by relaxing the upper esophageal sphincter (UES) which propels swallowed material from pharynx to stomach in a progressive and sequential manner

• Secondary Peristalsis– Involuntary waves– Caused by local distention in an attempt to clear the esophagus– Initiated in the smooth muscle of the lower esophagus

• Tertiary Peristalsis– Repetitive, nonprogressive and uncoordinated smooth muscle contractions

Normal Phases of Swallowing• Voluntary– oropharyngeal phase – bolus is voluntarily moved into the pharynx

• Involuntary– UES relaxation– peristalsis (aboral movement)– LES relaxation

• Between swallows– UES prevents air entering the esophagus during inspiration andprevents esophagopharyngeal reflux– LES prevents gastroesophageal reflux– peristaltic and non-peristaltic contractions in response to stimuli

Sphincters

• Upper esophageal sphincter (UES)– 3 cm long– Resting pressure: 20-60 mm Hg

• Lower esophageal sphincter (LES)– Not an anatomically defined sphincter in man– Called “zone of high pressure”– Serves to reduce gastric regurgitation and reflux– Located in the distal 3-5 cm of the esophagus– Normal resting pressure: 10-20 mm Hg

• Lower esophageal sphincter (Cont)– Pressure varies with respiration, increases with inspiration and drug/ hormone levels

– LES pressure is ↑ by:• Gastrin• Caffeine• α-adrenergic drugs• Bethanechol• Metoclopramide

– LES pressure is ↓ by:• Secretin• Cholecystokinin• Glucagon• Progesterone• Alcohol• Nitroglycerin• Nicotine• Anticholinergics• β-adrenergic drugs

– Intra-abdominal position of segment of esophagus maintained by phrenoesophageal ligament

Assessment of Esophageal Function

• Tests to detect structural abnormalities of the esophagus

• Tests to detect functional abnormalities of the esophagus

• Tests to detect increased esophageal exposure to gastric juice

• Tests of duodenogastric function as they relate to esophageal disease

Tests to detect structural abnormalities of the esophagus

• Radiographic evaluation –Barium swallow –Gastrografin swallow• Endoscopic assessment

Radiographic Evaluation ofEsophagus

• Contrast Media • Barium Sulfate – High density barium suspension is used in most institutions for double-contrast xrays of the upper GIT and mucosal relief views – Low density barium suspensions are additional materials used, as well as solid and semisolid bolus materials used in evaluation of dysphagia (eg. Barium- impregnated marshmallow, barium- soaked piece of bread, or a hamburger mixed with barium)


• Water contrast media – Iodinated water soluble Gastrografin should be employed whenever a perforation is suspected. – Disadvantages: • Do not coat the esophagus as well as barium sulfate solution → small abnormalities of mucosal surface are not demonstrated • Small perforation and slender fistula may be difficult to see since water soluble contrast media are of low density • Highly irritative and hyperosmotic → aspiration may induce laryngospasm; aspiration of large amounts may cause pulmonary edema


Single Contrast Techniques – Remains the basic radiologic method – Can be achieved in any patient in whom barium can be introduced into the esophagus even by intubation if necessary • Full column Technique • Mucosal Relief Technique

Double Contrast Technique

• Full Column Technique– Entails filling the esophageal lumen with barium and radiographing it in distended state– Patient is usually in the right prone or left supine oblique position while drinking barium suspension through a straw

Full Column Technique• Advantages: – Simple – Can demonstrate most of the important abnormalities of the esophagus: • Esophageal carcinoma • Esophageal strictures • Mucosal rings • Altered post-surgical anatomy– Can detect extrinsic lesions by virtue of displacement if they contact the wall of the distended esophagus

• Limitations: • inability to reliably show small or superficial mucosal abnormalities • It must always be supplemented with either double contrast or mucosal relief films to allow delineation of these more subtle abnormalities

Mucosal relief Technique• Provides a radiographic view of collapsed mucosal folds of esophagus coated with dense barium suspension or paste• Mucosal folds seen in this view should be smooth and without localized thickening or irregularity• Normal folds: measure 1-2mm in thickness in the completely collapsed esophagus• Abnormalities seen well with this technique: – esophageal varices – reflux esophagitis – infectious esophagitis – small neoplasms• The best means of demonstrating esophageal varices radiographically• Peptic strictures and mucosal rings usually require distention of esophagus and thus are not well shown by this technique

Double Contrast Technique• Accomplished by coating the esophageal mucosa with a dense barium suspension while distending the lumen with a combination of carbon dioxide and swallowed air

• Patient is examined in the upright position while ingesting carbon dioxide-producing granules with a small amount of water and then rapidly drinking a cup of high-density barium suspension

• Can show the mucosal surface of the esophagus in exquisite detail, and this is accomplished with the esophagus in the distended state;

• It combines the advantages of full-column and mucosal relief techniques• Limitations: – The patient must be able to cooperate and stand erect unaided – The patient must not have significant swallowing difficulties – After exclusion of patients with limitations, only about 75% of attempts of double contrast filming are successful → swallowed barium often pools in the distal esophagus preventing view of this important area – Timing is critical and transient esophageal distention that occurs may not be successfully captured on film

ALARM SYMPTOMS that indicate the need for upper endoscopy:

• Weight loss• Recurrent vomiting• Dysphagia• Bleeding• Anemia

Endoscopic Assessment of the Esophagus

Endoscopic evaluation is necessary to confirm or establish a diagnosis for most esophageal disorders, particularly when surgery is being considered

Indications:1. Upper abdominal symptoms that persist despite an appropriate trial of

medical therapy

2. Upper abdominal symptoms associated with other s/s suggesting worrisome organic dse (anorexia, weight loss, UGIB)

3. Patients >45y/o with new onset of abdominalSymptoms

4. Dysphagia or odynophagia

5. Persistent or recurrent esophageal reflux symptoms despite appropriate therapy6. Conditions in which presence of UGI pathology might modify planned management7. For confirmation and histologic diagnosis of radiographic lesions (eg. Ulcers, strictures, masses)8. Upper GI bleeding9. To assess acute injury after caustic ingestion10. Removal of foreign body11. Removal of selected polypoid lesions12. Placement of feeding or drainage tubes (oral, percutaneous endoscopic gastrostomy, nasojejunalfeeding tubes)13. Dilatation of stenotic lesions14. Palliative management of malignant dysphagia (eg. stent placement)15. Management of achalasia (eg. Botulinum toxin injection, pneumatic balloon dilatation)

Tests to detect functional abnormalities of the esophagus

• Stationary manometry• High-resolution manometry• Esophageal impedance• Esophageal Transit Scintigraphy• Video and Cineradiography

Stationary Manometry

• Esophageal manometry is the GOLD STANDARD for assessing esophageal motor function• The only modality that can define the pressure profile of peristalsis and allow measurement of LES pressure• Conventional manometry uses 3-8 sensors positioned at various points throughout the esophagus to measure the pressure changes that help assess the contractile pattern of the esophagus

Esophageal Manometry (EM)

Definition• Evaluation of esophageal muscularfunction (motility)

• EM concentrates on the lower 2/3 of• the esophagus (smooth muscle)

Esophageal Manometry (EM)

Procedure: what do we measure?• LES properties (static LES measurement) – Length – Resting pressure• Esophageal body (smooth muscle): – Contraction amplitude – Onset velocity• LES relaxation (dynamic LES measurement)

Procedure:• “pull-through” technique – Catheter pushed far into stomach (60 cm at nare)– Gradually pulled back to map LES

Esophageal Manometry (EM)LES “pull-through”

LES length – Total length – Intraabdominal length• LESP – “High pressure zone” (HPZ) – Highest pressure in LES at “rest “

Esophageal Manometry (EM)LES “pull-through”

Summary • LES length – Total length (3-5 cm) – Intraabdominal length (>1.5 cm)

• LESP (HPZ) –Mid-respiratory (10-45 mmHg) –End-expiratory (6-35 mmHg)

Esophageal Manometry (EM)Body motility

Procedure • Patient takes 10 swallows of water (5cc)

Measurements • Contraction amplitude • Peristalsis


Measurement • LES pressure during each swallow • LES starts relaxing as soon as a swallow starts


Summary

• LES pressure should drop below 8 mmHg


Summary• Contraction amplitude: 30 – 180 mmHg• Peristalsis: onset velocity < 8s

High Resolution Manometry

• Uses a catheter-based system with multiple sensors, typically 1 cm or less apart, at the level of UES and LES.

• The sensors should span from the pharynx to the stomach, eliminating the need to pull back the catheter to measure resting pressures, such as with conventional manometry.

• Pressure measurements are recorded both in the resting phase and during 10 consecutive swallows.

Indications for Esophageal Manometry

1. Dysphagia – for the assessment of functional disorders after structural disorders have been ruled out

2. Noncardiac chest pain – to assess for esophageal dysmotility as a cause of symptoms

3. Diagnosis or confirmation of suspected motility disorder

4. Preoperative assessment of esophageal motility prior to planned surgery

5. Postoperative assessment – to detect response to surgery or confirmation of response to treatment, or to assess the cause of persistent symptoms after surgery

Esophageal Impedance

• Method used to measure bolus transport by measuring the resistance to electrical conductivity of the esophagus and its contents• This test measures whether gas or liquids reflux into the esophagus.• Helpful for people who regurgitate substances that aren't acidic (such as bile) and can't be detected by an acid probe.• As in a standard probe test, esophageal impedance uses a probe that's placed into the esophagus with acatheter.

Normal bolus transitFor each swallow

• Total bolus transit time (TBTT) < 15 sec • Bolus clearance >5 sec

Esophageal Transit Scintigraphy

• Gastro-esophageal scintigraphy is a sensitive and quantitative, noninvasive technique for the analysis of esophageal transit time and gastro-esophageal reflux

• The esophageal transit of a 10-ml water bolus containing technetium-99m sulfur colloid can be recorded with a gamma camera

• Using this technique, delayed bolus transit has been shown in patients with esophageal motor disorders

Video and Cineradiography

• High speed cinematic or video recording of radiographic studies allows re-evaluation by reviewing the studies at various speeds

• More useful than manometry in evaluation of the pharyngeal phase of swallowing

• Loss of normal stripping wave or segmentation of barium column with the patient in recumbent position correlates with abnormal motility of the esophagealbody

Indications for Videoesophagram

• Globus sensation• Dysphagia• Nasal regurgitation• Noncardiac chest pain• Suspected postoperative complications

Tests to detect increased esophageal exposure to gastric juice

• 24-hour Ambulatory pH Monitoring• Radiographic Detection of Gastroesophageal Reflux

Tests of duodenogastric function

• Gastric Emptying• Gastric Acid Analysis• Cholescintigraphy• 24-hr gastric pH Monitoring

GastroesophagealReflux Disease

(GERD)and Hiatal Hernia

Gastroesophageal Reflux Disease(GERD)

• Any symptoms or esophageal mucosal damage that results from reflux of gastric acid into the esophagus

• Classic GERD symptoms–Heartburn (pyrosis): substernal burning discomfort–Regurgitation: bitter, acidic fluid in the mouth when lying down or bending over

Etiology of Reflux

• Decreased LES tone• Delayed gastricemptying• Increasedintraabdominalpressure due toobesity, tight garmentsor large meal• Motor failure ofesophagus with loss ofperistalsis• Iatrogenic injury to LES

Important Reasons to Diagnoseand Treat GERD

• Negative impact on health-related quality of life

• Risk factor for esophageal adenocarcinoma

Heartburn is Classic Symptom of GERD

• Substernal burning and/or regurgitation• Postprandial• Aggravated by change in position• Prompt relief by antacids

Extraesophageal Manifestations of GERD

PULMONARY ENT Asthma Hoarseness Aspiration pneumonia Laryngitis Chronic bronchitis Pharyngitis Pulmonary fibrosis Chronic cough Dysphonia Other Sinusitis Chest pain Subglottic stenosis Dental erosion Laryngeal cancer

Symptoms of Complicated GERD

• Dysphagia – Difficulty swallowing: food sticks or hangs up• Odynophagia – Retrosternal pain with swallowing• Bleeding – Hematemesis – Melena

When to Perform Diagnostic Tests

• Uncertain diagnosis• Atypical symptoms• Symptoms associated with complications• Inadequate response to therapy• Recurrent symptoms• Prior to anti-reflux surgery

Diagnostic Tests for GERD

• Barium swallow• Endoscopy• Ambulatory pH monitoring• Esophageal manometry

Barium Swallow

• Useful first diagnostic test for patients withdysphagia –Stricture (location, length) –Mass (location, length) –Bird’s beak –Hiatal hernia (size, type)

ENDOSCOPY

• Indications: – Alarming symptoms – Empiric therapy failure – Preoperative evaluation

Ambulatory 24hr pH Monitoring

• Physiologic study• Quantify reflux in proximal/distal esophagus – % time pH < 4 – DeMeester score

• Most sensitive test for GE reflux

Treatment Goals for GERD

• Eliminate symptoms• Heal esophagitis• Manage or prevent complications• Maintain remission

Lifestyle Modifications areCornerstone of GERD Therapy

• Elevate head of bed 4-6 inches• Avoid eating within 2-3 hours of bedtime• Lose weight if overweight• Stop smoking• Modify diet – Eat more frequent but smaller meals – Avoid fatty/fried food, peppermint, chocolate, alcohol, carbonated beverages, coffee and tea• OTC medications PRN

Acid Suppression Therapy forGERD

H2-Receptor Antagonists (H2RAs)• Cimetidine (Tagamet®)• Ranitidine (Zantac®)• Famotidine (Pepcid®)• Nizatidine• (Axid®)

Proton Pump Inhibitors(PPIs)

• Omeprazole (Prilosec®)• Lansoprazole (Prevacid®)• Rabeprazole (Aciphex®)• Pantoprazole (Protonix®)• Esomeprazole (Nexium ®)

Effectiveness of Medical Therapiesfor GERD

Treatment ResponseLifestyle modifications/ antacids 20%H2-receptor antagonists 50%Single-dose PPI 80%Increased-dose PPI up to 100%

Treatment Modifications for Persistent Symptoms

• Improve compliance• Optimize pharmacokinetics – Adjust timing of medication to 15 – 30 minutes before meals (as opposed to bedtime) – Allows for high blood level to interact with parietal cell proton pump activated by the meal• Consider switching to a different PPI

GERD is a Chronic Relapsing Condition

• Esophagitis relapses quickly after cessation of therapy

– > 50 % relapse within 2 months – > 80 % relapse within 6 months• Effective maintenance therapy is imperative

Complications of GERD

• Erosive/ulcerative esophagitis• Esophageal (peptic) stricture• Barrett’s esophagus• Adenocarcinoma• Schatzki’s ring

Erosive Esophagitis

• Gastric acid and pepsin are corrosive to mucosa• Acid-mediated reflux causes erosions.

EROSIVE ESOPHAGITIS

Peptic StrictureBarium Swallow Endoscopy

Peptic Stricture• A stricture is an• esophageal• narrowing, usually 13• mm or less in dm,• that causes• dysphagia.• Normal: up to 30 mm• in dm• Peptic strictures• are the endstage• result of chronic• reflux esophagitis.• Stricture formation• occurs in 7–23%• of patients with• reflux esophagitis.

Barrett’s Esophagus

• Mucosal metaplasia of distal esophagus, squamous to columnar• Associated with increased risk of developing adenocarcinoma (10-15%)• Correction of reflux does not prevent malignant transformation• Esophageal resection is indicated for severe dysplasia

Barrett’s Esophagus

Histologic Classification ofBarrett’s Esophagus

1.Nondysplastic BE/ Nondysplastic IM2.Low-grade dysplasia (LGD)3.High-grade dysplasia (HGD)4.indefinite for dysplasia

Schatzki’s Ring• Constrictive band at thesquamocolumnar junctioncomposed of mucosa andsubmucosa, not esophagealmuscle• The pathogenesis of Schatzkirings is not clear, and at least 4hypotheses have been proposed.1.The ring is a pleat of redundant mucosa that forms when the Esophagus shortens transiently or permanently for unknown reasons.2.The ring is congenital in origin.3.The ring is actually a short peptic stricture occurring as a consequence of gastroesophageal reflux disease.4.The ring is a consequence of pillinduced esophagitis.

Esophageal CancerBarium Swallow

Endoscopy

Goals of Surgical AntirefluxProcedures:

• Restore normal anatomy •Restore segment of intra-abdominal esophagus •Maintain distal esophagus as small diameter tube •Narrow the hiatus• Re-creating an appropriate high-pressure at the esophagogastric junction• Avoid increasing resistance of relaxed sphincter to a level that exceeds the peristaltic force of esophagus• Maintaining this repair in the normal anatomic position

Angle of His• The angle of His is theacute angle createdbetween the cardia atthe entrance to thestomach, andthe esophagus. It forms avalve, preventing refluxof duodenal bile,enzymes and stomachacid from entering theoesophagus, where theycan cause inflammation.

Surgical Antireflux Procedures

Fundoplication - Mobilise the lower esophagus and wrap the fundus of the stomach around it either totally or partially


• Nissen Fundoplication• Hill Fundoplication• Belsey Fundoplication• Angelchik Fundoplication• Collis Fundoplication

Surgical Antireflux Procedures- Total Fundoplication:- - Originally described byNissen in 1956- 360° fundal wrap around thedistal esophagus withdivision of the short gastricvessels (“floppy”)- Fundus is wrappedcompletely around theesophagus- Approach is either abdominalor thoracic

Surgical Antireflux ProceduresPartial Fundoplication(<360°): - Nissen cause an over competent GEJ responsible for the post-op dysphagia and gasbloat. - Belsey a 270° vertical fundoplication via a left thoracotomy - Toupet (posterior fundoplication) Recent review → no long-term difference in reflux control Less S/E ? Less short term dysphagia


- Hill’s posterior gastropexy- - Musculomucosal flap valve created by the angle of His against the lesser curve – an important barrier to reflux.- Phrenoesophageal ligament is anchored to the median arcuate ligament of the diaphragm and accentuating the angle of His.- Abdominal approach- 180°wrap- - Not popular → difficulty identifying the arcuate ligament.

Belsey Fundoplication

• Partial (270°) fundoplication performed via thoracotomy.• Exaggerated GE angle, stomach is anchored below the diaphragm

Dor Anterior Fundoplication

- Flinders group – first prospective randomised study of Anterior Fundoplication vs Nissen- (180° anterior wrap anchored to the right hiatal pillar and esophagus)- Less dysphagia & Flatulence- Trade-off → less effective reflux control

Toupet Belsey, Dor

Angelchik procedure

• silicon gel-filled,doughnutshapeddevice with atantalum tie strap thatwraps around the GEjunction below thediaphragm• Abdominal approach• Has an excessiveincidence of complicationssecondary to migrationand erosion and is nowgenerally avoided.

Complications of Antireflux Surgery

• Morbidity/Mortality • Hill -8%/4% • Belsey -14%/0.5% • Nissen -24%/1%• Excessively tight wrap → dysphagia• Excessively loose or short wrap → reflux• “Slipped Nissen” – when wrap slides down GEJ retracts into the chest, and the stomach is partitioned• “Gas bloat syndrome” – difficulty with eructationdue to a restored LES in a patient who swallows air

HIATAL HERNIA• Type I : Sliding or Axial• Type II: Paraesophageal (PEH) or Rolling Hernia/ Giant Hiatal Hernia• Type III: a combination of Types I and II• Type IV: hiatal hernia in which the colon herniates as well

Type I: Sliding/Axial

• GE junction migrates above the diaphragm• Upward dislocation of cardia in the posterior mediastinum• Phrenoesophageal membrane is intact; No true peritoneal sac• Most common hiatal hernia 90%• Significant only if with reflux symptoms• Etiology: – Chronically ↑intra-abdominal pressure – Weakness of supporting structures at esophageal hiatus

Type II: Paraesophageal Hernia or Rolling Hernia

• Characterized by an upwarddislocation of the gastricfundus alongside a normallypositioned cardia• GE junction is maintains itsnormal position• With peritoneal sac• Reflux rare• Uncommon type of hernia• Can result in gastric volvulusand strangulation• All type II hernias should berepaired

Type III: Mixed Hernia• Combined sliding-rolling hernia

• The end stage of type I and II hernias when the whole stomach migrates up into the chest by rotating 180° around its longitudinal axis, with the cardia and stomach as fixed points

• The abnormality then is referred to as an “intrathoracic stomach”

type 3 hiatal hernia with anterior organoaxialrotation. Mobile greater curve moves anteriorly and

superiorly so that in 180° organoaxial rotation,mirror image of stomach is created with convexgreater curvature located above and to right of

concave lesser curvature.

Mirror imagestomach

Type 3 paraesophageal hernia with 180°mesenteroaxial rotation is shown. Rotation of

stomach is shown along axis (dotted lines)perpendicular to organ's long axis (solid line).

TYPES OF HIATAL HERNIA

ESOPHAGEAL MOTILITYDISORDERS

Esophageal Motility Disorders

• Are classified as functional disorders because they interfere with a normal act of swallowing or produce dysphagia without any associated organicobstruction or extrinsic compression

• Information from esophageal manometry is extremely helpful - Some conditions are indistinguishable by xrays (barium) but have specific manometric characteristics

Disorders of Esophageal Motility

• Upper esophageal sphincter (UES) dysfunction – Cricopharyngeal Achalasia – symptoms occur when there’s difficulty propelling liquid or solid food from the oropharynx into the upper esophagus – Caused by abnormalities in central and peripheral nervous systems, metabolic, inflammatory neuropathy, GERD, and others – Patients complain of “lump in the throat”, excessive expectoration of saliva, weight loss and intermittent hoarseness

Dx and Tx of CricopharyngealAchalasia

• Barium swallow may be normal especially inpatients with intermittent symptoms

• Esophageal function studies (manometric and acid reflux testing) should be performed whenever possible

• In patients with severe symptoms and no reflux, surgical intervention may be necessary

• Tx depends on cause- antireflux procedure, bougienage, cervical esophagotomy

Motor Disorders of the Body ofthe Esophagus

• Esophageal motor disorders range from hypomotility (achalasia) to hypermotility (diffuse spasm)• Achalasia is defined as a failure or lack of relaxation of LES – The name focuses on the distal sphincter however the condition involves the entire esophageal body• Diffused esophageal spasm is poorly understood and poorly treated

Achalasia

• The etiology is not known

• The characteristic clinical, radiographic and manometric findings have occurred following a variety of situations: – Severe emotional stress – Major physical trauma – Chagas’ disease

• Hallmark pathologic feature: decreasednumber of inhibitory ganglion cells in Auerbach's plexus at all esophageal levels.

Achalasia

• The classic triad of symptoms include dysphagia, regurgitation and weight loss

• Manometric findings: Increased LES resting pressure Decreased LES relaxation Decreased esophageal peristaltic activity

Achalasia

• Retrosternal pain on swallowing (odynophagia) is not characteristic

• Effortless regurgitation after eating especially upon bending forward is usually not associated with a sour taste of undigested food-in contrast to acid regurgitation

• Coughing spells at night

• Often results in recurrent respiratory symptoms due to aspiration pneumonitis (spillover pneumonitis)

• Is a premalignant esophageal lesion with carcinoma developing as a late complication in patients who have this condition an average of 15-25 years

Radiographic Appearance of Achalasia

• Varies with the extent of the disease • EARLY STAGE: Mild dilatation • LATER STAGES: Massive dilatation and tortuosity • Peristalsis is disordered in early stages and lacking in later stages • The radiographic hallmark: distal bird-beak taper of the (EG) junction

ACHALASIA

Tests for Achalasia

• Manometric criteria of achalasia: – failure of the LES to relax with swallowing – lack of progressive peristalsis throughout the length of the esophagus

• Esophagoscopy is indicated an achalasia to rule out severe retention esophagitis, carcinoma or tumor of the cardia (stomach) that mimics achalasia

Treatment for Achalasia

• Treatment is palliative – Nonsurgical – Surgical – Both are directed toward relieving the obstruction caused by the nonrelaxing LES

Nonsurgical Treatment of Achalasia

• • Early stages• –Sublingual nitroglycerin• – Long-acting nitrates• –Calcium channel blockers• – Endoscopic options:• • May be the most effective initial nonsurgical• treatment for achalasia• 1.Passage of Mercury weighted bougies• • 65% improve with pneumatic or• hydrostatic dilation• 2. Botulinum toxin injections into the LES

Surgical Treatment

• Esophagomyotomy • First described by Ernest Heller in 1913• Abdominal approach with anterior and posterior myotomy of LES

Diffuse Esophageal Spasm (DES)

• Is poorly understood hypermotility disorder – Results from repetitive high amplitude esophageal contractions• The etiology is unknown• These patients typically are anxious and complain of chest pain inconsistent to eating, exertion and position• The character of pain may mimic that of angina• Symptoms are greatest during periods of emotional stress• Patients may experience slow emptying of the esophagus and obstructive symptoms are uncommon

Radiographic Findings

• Frustratingly variable – Classic “corkscrew” – Beaklike taper – Increase in esophageal wall thickness

Diffuse Esophageal Spasm

Testing

• Esophagoscopy– Distal esophageal obstructing lesions may produce proximal esophageal contractions that are confused with DES• Esophageal manometry• Diagnostic when present – Classic criteria are: • Simultaneous, multiphasic, repetitive, high amplitude contractions that occur after a swallow

Treatment for DES

• Due to the lack of understanding of this condition the treatment is less than satisfactory• Tx includes small soft meals, calcium channel blockers, and extended esophagomyotomy• Antispasmodics are occasionally helpful• Response to sublingual nitroglycerin is variable

Scleroderma

• Fibrous replacement of esophageal smooth muscle and atrophy• Etiology is unknown• Characterized by induration of skin, fibrous replacement of smooth muscle of internal organs and progressive loss of visceral and cutaneous function• LES loses tone and normal response to swallowing• Disruption of esophageal peristalsis is common• Esophageal manometry and intraesophageal pH readings are the most sensitive means of detection

Treatment for Scleroderma

• Medical and surgical tx is directed at antireflux measures to decrease esophagitis

• Standard antireflux medicine includes H-2 blockers – Cimetidine – Ranitidine

• In patients with intractable symptoms gastroesophageal reflux surgery should be considered

Diverticula of the Esophagus

Esophageal Diverticula

• Almost all are acquired and occur predominantly in adulthood• Are classified according to their: – Site of occurrence• Pharyngoesophageal• Parabronchial• Epiphrenic – Wall thickness• True• False (contains only mucosa and submucosa) – Mechanism of formation• Pulsion (created by elevated intraluminal pressure)• Traction

Pharyngoesophageal Diverticula(Zenker)

• The most common esophageal diverticulum• Occurs between the ages of 30-50 (believed to be acquired)

• Arises within the inferior pharyngeal constrictor, between the oblique fibers of the thyropharyngeus muscle and the cricopharyngeus muscle

• Is a pulsion diverticulum

• Complaints are of cervical dysphagia, effortless regurgitation of food or pills, choking, recurrent aspiration

• Sometimes a gurgling sensation in the neck after swallowing is felt

Zenker’s Diverticulum

Diagnosis and Treatment

• Barium swallow establishes the diagnosis• Surgery is indicated in symptomatic patients regardless of the size – It is the degree of cricopharyngeal muscle dysfunction and not the size of the diverticulum that determines the relative severity of cervical dysphagia• Treatment includes diverticulectomy with myotomy of cricopharyngeus muscle

Midesophageal (Traction)Diverticula

• • Are typically associated with mediastinal• granulomatous disease (TB, histoplasmosis)• • Mediastinal granulomatous disease of adjacent• lymph nodes adhere to the esophagus and pull• on wall during healing• • These are usually an incidental finding on• barium swallow• • They tend to be very small and rarely cause• symptoms or require treatment• • Need to be differentiated from pulsion• diverticula which can also occur in this location• (associated with neuromotor esophageal• dysfunction)

Midesophageal (Traction)Diverticula

Epiphrenic (Supradiaphragmatic)Diverticula

• Located within the distal 10cm of the thoracic esophagus

• Pulsion type, arise due to distal obstruction or esophageal motor dysfunction

• Many patients are asymptomatic when diagnosed

• When symptomatic their symptoms are difficult to differentiate from: hiatal hernia, DES, achalasia, reflux esophagitis and carcinoma

• Dysphagia and regurgitation are common symptoms

Epiphrenic (Supradiaphragmatic)Diverticula

Diagnosis and Treatment

• Diagnosis is easily made with barium swallow

• Esophageal function studies should also be performed to rule out any motor disturbances

• Lesions < 3 cm often require no treatment

• Large and those with extreme symptoms require surgical repair

Epiphrenic Diverticulum

TUMORS OF THEESOPHAGUS

Benign Esophageal Tumors andCysts

• Benign tumors are rare (< 1 %)• Classified in two groups – Mucosal – Extramucosal (intramural)

• More useful classification: – 60% of benign neoplasms are leiomyomas – 20% are cysts – 5% are polyps – Others (< 2 percent)

Leiomyomas• Most common benign tumor of the esophagus• Intramural in the circular muscle layer• Average age at presentation is 38; twice as common in males• 90% occur in lower 2/3 of esophagus• Obstruction and regurgitation may occur in large lesions• Dx: – barium swallow is the most useful method – CXR – endoscopy• Tx: majority can be removed by simple enucleation; large tumors or those involving the GEJ may require esophageal resection

Esophageal Cysts

• Arise as diverticula of the embryonic foregut of this cyst present in childhood

• Over 60% are located along the right side of the esophagus

• Enteric and bronchogenic cysts are the most common

• 60% present in the first year of life with either respiratory or esophageal symptoms

• Cyst found in the upper third of the esophagus present in infancy while lower third lesions present later in childhood

• Surgical excision by enucleation is the preferred treatment

Pedunculated IntraluminalTumors (Polyps)

• Benign polyps are rare

• Usually occur in older men and may cause intermittent dysphagia

• Are sometimes easily missed with barium swallow and esophagoscopy

Malignant Tumors of theEsophagus

• Usually are in advanced stages at the time of diagnosis (involving the muscular wall and extending into adjacent tissues)

• Alcohol consumption and cigarette smoking seem to be the most consistent risk factors

• Esophageal squamous cell carcinoma (95% of all esophageal cancers) is a disease of men (5: 1)

• Squamous cell esophageal cancer occurs least frequently in the cervical esophagus and

• Squamous cell esophageal cancer occurs most often in the upper and midthoracic segments

Malignant Tumors of theEsophagus

• Adenocarcinoma constitute approximate 8% of primary esophageal cancers• Most often occur in the distal third of the esophagus in the 6th decade of life, but now occurs not only more frequently but in younger patients and is often detected at an earlier stage• Male to female ratio is 3:1• Patients with Barretts metaplasia are 40 times more likely to develop adenocarcinoma• These tumors are aggressive as well

Clinical Presentation

• Dysphagia is the presenting complaint in 80-90% of patients with esophageal carcinoma

• Early symptoms are sometimes nonspecific retrosternal discomfort or indigestion

• As the tumor enlarges, dysphagia becomes more progressive.

• Later symptoms include weight loss, odynophagia, chest pain and hematemesis

Diagnosis

• Barium swallow has 92% accuracy – Identify abn peristalsis, mucosal irregularity and annular constructions

• Fiberoptic endoscopy with biopsy and washings is confirmatory in 95% of cases

• Bronchoscopy with biopsyto r/o involvement of bronchus in upper 2/3 tumors and synchronous lung primary

• Nasopharyngoscopy and direct laryngoscopy to r/o synchronous head and neck lesions and vocal cord involvement

• CT scan of chest with extension to liver and adrenals to assess tumor spread

Staging of Tumors• Endoscopic ultrasound-to define the depth of invasion and presence of paraesophageallymph nodes

• Chest x-ray ± abnormal findings

• CT scan (most widely used and now standard radiographic means of a staging)

• Bronchoscopy for tumors which are proximal to the trachea

The TNM classification

• (a) “T” (depth of invasion of the primary tumor).

• (b) “N” (regional lymph involvement).

• (c) “M” (presence or absence of distant metastases).

Primary Tumors (T)

• Tx Primary tumor cannot be assessed (cytologically positive tumor not evident endoscopically or radiographically)

• T0 No evidence of primary tumor (e.g., after treatment with radiation and chemotherapy)

• Tis Carcinoma in situ• T1 Tumor invades lamina propria or submucosa, but not

beyond it• T2 Tumor invades muscularis propria• T3 Tumor invades adventitia• T4 Tumor invades adjacent structures (e.g., aorta,

tracheobronchial tree, vertebral bodies, pericardium)

Regional Lymph Nodes (N)

A. Nx Regional nodes cannot be assessedB. N0 No regional node metastasisC. N1 Regional node metastasis

Distant Metastasis (M)

1. M0 No metastasis2. M1 Distal metastasis

Stage Grouping

STAGE T N M

Stage 0 Tis N0 M0

Stage I T1 N0 M0

Stage IIA T2T3

N0N0

M0M0

Stage IIB T1T2

N1N1

M0M0

Stage III T3T4

N1N1

M0M0

Stage IV Any T Any N M1

Treatment

• Local tumor invasion or distant metastatic disease precludes cure.• Esophageal Ca is a systemic disease when it is diagnosed; local therapy (radiation or operation) is simply unable to eradicate this malignancy.• The 5-year survival rate in Western countries from esophageal Ca treated by either radiation or surgery is generally < 10%• More than 80% of the patients die within 1 year of diagnosis. Consequently, until very recently, the primary aim of therapy for esophageal carcinoma has been palliation (restoring the patient's ability to swallow).• Esophageal Ca is notorious for its ability to spread in the submucosal lymphatics well beyond the gross extent of the tumor• Resection to clear margins are therefore desirable to minimize the possibility of recurrent tumor at the anastomotic suture line.

Surgery

• Resection provides the best palliationfor most patients with localizedcarcinoma.

• Esophageal resection and reconstructionremain formidable operations in patientswhose nutritional and pulmonary statushave been compromised by impairedswallowing.

SurgeryLeft thoracoabdominal incision – Is the approach to distal esophageal Ca. – Distal esophagus, proximal stomach, and adjacent LN-bearing tissues are resected, and intrathoracic esophagogastric anastomosis is performed. IVOR-LEWIS ESOPHAGECTOMY – high intrathoracic esophagogastric anastomosis is performed. In either case, a gastric drainage procedure (pyloromyotomy or pyloroplasty) is recommended to prevent subsequent postvagotomy gastric outlet obstruction due to pylorospasm. – approach for higher thoracic esophageal tumors Transhiatal esophagectomy without thoracotomy (limited exposure of the intrathoracic esophagus and its blood supply and the risk of hemorrhage and the inability to carry out a complete mediastinal lymph node dissection ).Laryngopharyngocesophagectomy. For treatment of Ca involving the cervicothoracic esophagus (and frequently the larynx).

Transhiatal esophagectomy without thoracotomy

• Cervical (arrowhead) and upper abdominal midline (arrow) incisions are made.

• Mobilization of the stomach foresophageal replacement is performed through a laparotomy with pyloroplasty.

• The esophagus is mobilized fromthe back wall of the tracheathrough the cervical incision.

• From below, the surgeon’s handpasses through the widened hiatus.Any remaining attachments of themuscular esophageal tube areavulsed from the esophageal wall.

Transhiatal esophagectomy without thoracotomy

Disadvantages:• limited exposure of the intrathoracic esophagus & its blood supply• the risk of hemorrhage• the inability to carry out a complete mediastinal lymph node dissection

Transhiatal esophagectomy withoutthoracotomy (Orringer Technique)

• The cervical esophagus is clamped,leaving adequate length forreconstruction• The esophagus is then extracted fromthe mediastinum.• The stomach is divided at the proximalregion with a stapler or clampPyloromyotomy is performed at thedistal portion• Remaining portion of the stomach isadvanced to the neck for esophagogastric anastomosis.

Left thoracoabdominalesophagectomy

• the approach todistal esophageal Ca• Distal esophagus,proximal stomach,and adjacent LN-bearingtissues areresected• intrathoracicesophagogastricanastomosis isperformed.

IVOR-LEWIS ESOPHAGECTOMY

• approach for higherthoracic esophagealtumors• high intrathoracicesophagogastricanastomosis isperformed• In either case, agastric drainageprocedure(pyloromyotomy orpyloroplasty) isrecommended toprevent subsequentpostvagotomy gastricoutlet obstruction dueto pylorospasm.

Chemotherapy

• • No data proved that chemotherapy alone provides improved• survival or palliation. Partial response, not long-term• remission, is the rule• • Single-agent chemotherapy used to treat many patients• with esophageal Ca who present with distant disease, with• cisplatin, mitomycin, and 5-fluorouracil achieving reported• response rates of 35%.• • Combination chemotherapy regimens such as:• • cisplatin, bleomycin, and vindesine or methotrexate;• • cisplatin, mitoguazone, and vindesine or vinblastine; and• • cisplatin and 5-fu used for metastatic or unresectable• esophageal Ca, with reported response rates of 11-55%• for 3-9 months.• • Combination chemotherapy has been used preoperatively in• a combined modality approach to esophageal Ca in hopes of• controlling occult metastatic disease and improving the• resectability rate.

• Multimodality therapy• • Because most patients have systemic or• locally invasive disease that precludes cure,• there is efforts to improve survival with• multimodality therapy.• • Experience with combined preoperative• radiation therapy and chemotherapy, as• well as preoperative chemotherapy and• postoperative adjuvant radiation, are• encouraging.• • This therapy provide better local-regional• control of the tumor than can be achieved by• radical resection of the esophagus alone

• Transoral intubation• • Uses a variety of tubes (Souttar, Mackler,• Mousseau, Fell, and Celestin) and the• Wilson-Cook and self-expanding stents,• have been used to provide palliation.• • Esophageal intubation carries an overall• reported mortality that ranges from 3-15%• and a complication rate of 20%.• • Complications:• 1. perforation of the esophagus• 2. migration of the tubes• 3. obstruction of the tubes by food• or tumor overgrowth.

• • Endoscopic laser therapy improves• dysphagia, but multiple treatments are• required and long-term benefit is• seldom achieved.• • Palliative internal bypass. Bypass of• unresectable Ca with colonic• interposition, gastric tubes or• retrosternal gastric bypass as a method• of palliation. These procedures are of• considerable magnitude and carry a high• mortality rate and survival in these• patients’ averages < 6 months.

• Preoperative Preparation for• Esophagectomy• • Pulmonary physiotherapy.• • Abstinence from cigarette smoking and use of an• incentive inspirometer.• • Antibiotics for associated pneumonitis may be• required.• • Nutritional build-up.• • Oral hygiene• • Barium enema should be done, if there is a history of• prior gastric operations that may preclude the use of• the entire stomach as an esophageal substitute, to• assess the suitability of the colon for esophageal• replacement. The colon should be prepared in the• event that a colonic interposition is required.

Esophageal Ruptureand

Perforation

Causes of Perforation

Iatrogenic –most common! Spontaneous -Endoscopy -Postemetic -Dilators -Esophageal intubation Radiation therapy -Variceal sclerosis Traumatic - Blunt and penetrating - CausticIntraoperative Carcinomas -Mediastinoscopy -Thyroid surgery

Clinical Presentation

• Symptoms and signs vary with the cause and location of the perforation• Pain is the most consistent symptom (70-90%)• Blood tainted emesis is present in 30% of these patients• The pain pattern is often misdiagnosed as a dissecting aortic aneurysm, spontaneous pneumothorax or myocardial infarction• Tachycardia and tachypnea is common• Hypotension and shock can occur

Diagnosis

• Chest x-ray (plain film) – When obtained early may appear normal – Mediastinal emphysema may appear in one hour – Pleural effusions may take several hours• Definitive diagnosis-contrast studies• CT scan’s for atypical presentations• Esophagoscopy is rarely used for diagnosis of perforation

Treatment

• Three factors affect management of esophageal perforation – Etiology – Location – The delay between rupture and treatment• Surgical treatment remains the mainstay of management in esophageal perforations

Treatment

• Early recognition and treatment are essential to survival• Basics: – Drainage – NPO – Fluid resuscitation – Broad spectrum antibiotics – Nutritional support in recovery period parenteral• nutrition is preferred

Nonoperative Treatment

• Controversial; Only recommended for: – Small perforation – Cervical perforation – Contained leak – No evidence of sepsis – Wide drainage back into the esophagus

• Nasogastric suction, antibiotics, close observation

Treatment Based onLocation of Perforation

• Cervical – Limited extravasation and extrathoracic perforation may initially be managed nonoperatively – Patients with crepitus or increased extravasation• Operative drainage• Antibiotics• Closure of rupture if possible• Cervical esophagostomy

Treatment Based onLocation of Perforation

• Thoracic – Mortality is 10-15% if treated within 24 hrs of injury; Increases to >50% if dx is delayed >24 hrs – Early: Suture closure, wide drainage, antibiotics; Repair with patch is controversial – Late:• Operative drainage and antibiotics• Suture closure is unlikely to hold• Some do esophagectomy, oversew cardia,create cervical esophagostomy

Complications of EsophagealPerforation

• Sepsis• Abscess• Fistula• Empyema• Mediastinitis• Death

Caustic Injuryto Esophagus

Causes of Corrosive Injury

1. Alkalis: – Most cases of caustic injury in western countries – Cleaning agents (NaOH), drain openers, bleaches, toilet bowel cleaners, and detergents…

2. Acids – Less frequently in western countries; more common in countries like India (glacial acetic acid) – Toilet bowel cleaners ( sulfuric, hydrochloric ), anti rust compounds ( hydrochloric, oxalic, hydrofluoric), swimming pool cleaners

Pathophysiology

1. Alkali-induced injury: – Liquefactive necrosis – 1-2 days: Thrombosis of small vessels – 2-4 days : Newly forming blood vessels , fibroblasts migration – 4-7 days: Mucosal sloughing, bacterial invasion, inflammatory response, and development of granulation tissue – > 2 weeks: Collagen deposition – > 3 weeks: Scar retraction => may continue for several months

2. Acid-induced injury: – Superficial coagulation necrosis – Thromboses the underlying mucosal blood vessels and consolidates the connective tissue => Protective eschar

ENDOSCOPIC GRADING OF ESOPHAGEAL AND GASTRIC BURNS

1. First-degree: • Mucosal hyperemia and edema2. Second-degree • Mucosal and sub-mucosal damage • Ulcerations, exudates, vesicle formation, granulation,fibroblastic reaction • Pseudomembrane formation • Scar formation3. Third-degree • Sloughing of mucosa • Deep ulcers • Massive hemorrhage • Complete obstruction of lumen by edema • Charring/ black eschar • Perforatiom

Clinical Presentation1. Vary widely – Hoarseness, stridor, dyspnea => Airway evaluation – Perforation: (During first 2 weeks) • Retrosternal or back pain • Localized abdominal tenderness, rebound, rigidity, Psoas sign, obturator sign • Massive hematemesis – Dysphagia, odynophagia, drooling, nausea, vomiting

2. Early signs and symptoms may not correlate with the severity and extent of tissue injury

3. Oral and oropharyngeal burns (pseudomembranes)

4. In absence of perforation, acute manifestations resolve ina few days; clinical improvement may continue for several weeks until course complicated by stricture.

Diagnosis

• • Esophagogastroscopy to establish• severity of injury• • Contrast exam of esophagus can• demonstrate injury as well as• suspected perforation

Initial Treatment

• Treatment of caustic lesion is directed toward management of both immediate and late consequences of the injury.• NPO• IV hydration• Broad spectrum antibiotics• Use of corticosteroids to attempt to limitstricture debatable

Operative Treatment

• Patients with evidence of esophageal or gastric perforation require immediate operation – Best explored through abdominal incision – Restoration of alimentary continuity should await resolution of acute insult• Stricture formation tends to be the rule – Dilatation is traditional therapy• Stricture that cannot be dilated or remains refractory after 1 year requires esophageal substitution – Stomach is the referred substitute but often unusable secondary to scarring from original injury – Esophagus should be excised

esophagus & diaphragmatic hernia

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