Benignesophagealdisorders

7/29/2019 Benignesophagealdisorders

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10-30% of patients with suspectedangina don't have coronary

disease.

From these 50% will haveoesophageal disorders.


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Anatomy

- Muscular tube - Conduit from the pharynxto the stomach

- C6 (Cricoid cartilage) to below thediaphragm

- From the incisor 40-45 cm (actual 20-25cm)

- Passes behind aortic arch and left main

bronchus.- Enters abdomen through oesophageal

hiatus 2-4 cm below the diaphragm


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Anatomy

- Held in position by:

. Reflection of the peritoneum onto the

stomach. Phreno-oesophageal ligament to the

oesophagus .


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Anatomy

Three area of narrowing- Cricopharangeus

- Behind the aortic arch

- LOS (thickening of the circularmuscles ~ 4cm)

The muscles upper 1/3 of oesophagus isstriated, remainder is smooth muscle

peristalsis wave 4-6cm/s (reflex regulatedin the medulla)


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Arterial supply:

Upper inferior thyroid arteryMiddle Bronchial arteries and

oesophageal branches directly from aorta

Lower L inferior phrenic and gastric

Venous drainage:

Upper oesophageal venous plexus toazygos vein

Lower oesophageal branches of thecoronary vein, a tributary of the portal

vein


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Histology:

- Stratified columnar epithelium withscattered mucus glands

- No serosa hence does not heal as well asthe rest of GIT

- Lower Oesophageal Sphincter (LOS)

Contraction: -adrenergic & cholinergicGastrin

Relax: -adrenergic,VIP and NO

CCK & glucagon


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Symptoms:

- Dysphagia: difficulty swallowing- Odynophagia: pain on or painful

swallowing

- Globus: lump in the throat- Heart burn: Stomach/Substernal burningsensation radiating up to the neck andrelieved acutely (but transiently) by

antacids


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Oesophageal Motility Disorders(1)

(i) Achalasia

(ii) Others

Diffuse oesophageal Spasm

Nutcracker Oesophagus

Hypertensive LOS

Scleroderma & other collagen-

vascular disorders (eg CREST)(The panels comments were:

Although they do see few Achalasias a year, they rarely see anyof the other disorders )


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- 3-5% of motility disorders- Normal peristalsis + Spontaneous

contraction + increase in LOS pressure

- Aetiology is unknown, ? defect in neuralinhibition normally mediated by NO

- Hypersensitive oesophagus

- Dx on Manometry- Endoscopy is unremarkable & Ba Swallowis N or disorganised (Corckscrew)


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Nutcracker Oesophagus

- High amplitude peristaltic waves(>180mmHg) prolonged (>6s)

- Endoscopy unremarkable but Endo USshows thickening of muscularis propria

- Higher incidence of psychiatric disorders

Hypertensive LOS

- Elevated LOS pressure (>45mmHg) withnormal peristalsis

- LOS relaxation is normal


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Treatment

- Medical Rx effective in 80%- Agents acting on Smooth Muscle (eg

Nitrates, Ca channel blockers),

- Psychoactive agents (eg Benzodiazepines,Tricyclics) (?more effective)

- Botox injection

- Surgical Rx, reserved for Px with dysphagiaand poor oesophageal emptying

Myotomy (Lap / Thoracoscopic)


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Ineffective motility

- Scleroderma (80% of Px), other CollagenVascular disorders (SLE, RA, MCTD),

Amyloidosis, Alcoholism, MS, myxoedema

etc- Affect the myenteric plexus + fibrosis and

vascular obliteration (Predominantly distal

SM)- or absent peristalsis and LOS pressure


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Achalasia

- Uncommon (0.5-1 in 100,000), M=F, 20-50s- Ineffective relaxation of the LOS combinedwith loss of oesophageal peristalsis impaired oesophageal emptying and

gradual dilatation- or loss of inhibitory myenteric ganglion

cells & progressive neural fibrosis

- Also decreased production of NO & VIP

- Slight increase risk of SCC


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Achalasia - Presentation

- Dysphagia - delayed and progressivepresentation (mean 2 years)

- Stress or cold fluid exacerbates symptoms

- Spontaneous or forced regurgitation ofundigested food

- 10% will have pulmonary complication

- Can have heartburn (not GORD)

- Chest pain ( heartburn) - 30-50% resolveswith Myotomy


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Achalasia - Diagnosis

- Air fluid levels on plain Xray- Ba swallow: dilated oesophagus with Bird's

beak tapering

- Manometry is gold standard

. Resting LOS pressure is usuallynormal (may be elevated)

. Complete absence of peristalsis

- Endoscopy: dilated oesophagus with tightlyclosed LOS gentle pressure will admitthe scope with a "pop.


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Achalasia - Diagnosis


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Achalasia - Treatment

- Palliation of dysphagia relieve functional obstruction of distaloesophagus (neuromuscular defect is notcorrected)

o Medical (Nitrates and Ca channelblockers)

. Poorly absorbed, inconsistent andshort lived effect

. SE.


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- Botox injection: bind to cholinergicnerves and irreversibly inhibit AcetylCholine release

- 60-85% of patient get relief but 50% get

recurrent symptoms within 6 months.- Efficacy decreased with repeated injection

- Expensive

- Cause intense inflammatory reaction whichwill make subsequent surgery moredifficult and increase risk of perforation.

(Prof Hunt thought this was a theoretical problem and in practicehe did not find surgery more difficult)


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- Graded pneumatic dilatation (underfluoroscopy)

Tears the muscle (myotomy)

30mm for 1-3min (day procedure)Can have repeated dilatation

60-90% success rate

Efficacy is decreased after seconddilatation

perforation rate ~ 2%


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AchalasiaSurgical treatment

- Originally performed by Ernest Heller in1914 for Achalasia

Two myotomies: anterior and posterior

- Modified Heller: anterior only- Excellent results in 90-95%

- Traditionally trans-thoracic or trans-abdominal

- Now minimally invasive Laparoscopic /Thoracoscopic


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AchalasiaSurgical treatment

- ControversiesLength of myotomy

Proximal 5-7 cm above GOJ

? evidence(1) longer gastric myotomies(>3cm) better relief from dysphagia

Need for antireflux procedure as well(The panel thought everyone should do an antireflux procedure,

but the length and proximal extension of the myotomy is not

as important.)


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Benign oesophageal tumours

- From any layer- Mucosal: . Papillomas (sessile or

pedunculated)

- Intramural: . Leiomyoma, FibromaLipoma

. Congenital cysts or

reduplication (lower)


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Benign oesophageal tumours

- Asymptomatic or may be large enough toencroach the lumen

- Peristalsis is normal with Leiomyoma, but

spasm with cysts and reduplication- Intraluminal lesions Dx on Endoscopy

(should Bx)

- Intramural lesions Dx Radiologically(smoothly rounded) should not be Bx


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Gastro-oesophageal reflux disease

- Reflux of gastric content is normal- GORD is when affects patients well being

. Symptoms

. Physical complications

- Common - (difficult to assess - Px self treat)

- 75% of oesophageal disease in clinicalpractice

In the US(2)40% monthly14% weekly (15-20% Australia)

7% daily


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- Normal gastric emptying- Adequate oesophageal clearance

- Contributing Factors:

Familial, Obesity, Diet (Fat, Chocolate,Caffeine), Smoking, Drugs

- Hiatus hernia 85% of Px with reflux have asliding hernia

But most people with a sliding hernia donthave disabling symptoms


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SymptomsMild / Severe

- Heartburn (also in PUD and 40% IBS Px)

- Regurgitation of previously ingested food

- Waterwash (saliva production)

- Dysphagia (defective peristalsis / stricture)

- Odynophagia (severe oesophagitis)

- Haematemesis


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ComplicationOesophageal: Oesophagitis

Barretts (10%)

Strictures (Panel: very rare now)

Adenocarcinoma

50% of Px with GORD get complications


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ComplicationExtra-oesophageal: Laryngitis

Pharyngitis

SinusitisPulmonary

Adult onset asthma

NB Poor correlation between frequency andseverity of symptoms and prevalence ofcomplication


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GESA recommendation for Mx:Mild symptoms

- Antacids /over the counter H2 antagonists

- Lifestyle changes:Diet (Fatty, Spicy, Coffee, Acidic)

ETOH (moderation OK)

Smoking

Late/large meals & early recumbency

Drugs

Tight clothes


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GESA recommendation for Mx:Moderate to severe symptoms

- First line Rx: 2-4/52 of double dose PPI

(Superior to endoscopy for Dx)- Symptomatic control equates to

endoscopic healing (even LA GradeC&D)


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GESA recommendation for Mx- Further Ix if:

Unclear Dx

Symptoms persist/progress on RxComplicated Symptoms

Suggestion of other pathology (Ca,

PUD, infective/drug inducedoesphagitis)


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GESA recommendation for Mx- Further Ix:

Endoscopy

Negative in >50% of Px with GORDIdeal for:

- Dx and grading of oesophagitis

- Other mucosal lesions- Dx and Rx strictures

- Dx of Barretts


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GESA recommendation for Mx- Further Ix:

24/24 ambulatory oesophageal pH

monitoringpH 1 hours


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GESA recommendation for MxTrial of withdrawal of therapy

Majority will have symptom relapse

Repeat course of the previous RxFollowed by on demand H2 antagonist/ PPI antacids

a small proportion will be symptom free Majority continuous treatment / Surgery


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Few topics of interest

- Barretts oesophagus

- Dysplasia- H Pylori

-Non-Acidreflux


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Gastro-oesophageal reflux diseaseBarretts

-Transformation of pseudostartified tocolumnar epithelium

- If gastric or pancreatic (rarer) no riskof AdenoCa

(The panel thought it is important to emphasise on non-acidsecreting gastric mucosa is in the cardia and can extendupwards without risk of adenoCa)

- Specialised intestinal metaplasia risk ofAdenoCa (much less if length


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Barretts- Once present no evidence that Acid

suppression will reverse progression todysplasia

- Recent study showed in Px with Barrettsthere is progression after antireflux

surgery(3).

- Also increased evidence in the role if Bilesalts in Barretts(4).


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Non-Acid reflux(5)

- Animal studies have shown: Acid alonerequires high concentration to damage theoesophageal mucosa

- Oesophagitis has been observed inachlorhydric patients

- Duodenogastro-oesophageal reflux

(DGOR) is the reflux of duodenal content(bile acids and pancreatic secretions) intothe stomach (normalpostprandially and

nocturnally)


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Non-Acid reflux(5)

- Contains trypsin as well as bile acids andcan occurs at neutral and acidic pH too

- Conjugated Bile salts @ low pH,Unconjugated bile salts and trypsin @ highpH can damage mucosa

- Clinical studies: There is evidence that

mucosal damage increase with increasedexposure to the duodenogastro-oesophageal reflux.


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Non-Acid reflux(5)

- Investigations

. Scintigraphy(injection ofTc99m @

5 min interval Camera for 60/60 can show duodenal reflux

. Bilitec2000 is spectrophometry,measure the bilirubin concentration in

the oesophagus. (can have ambulatorymonitoring)

Problem with very low pH, food &

mucosal folds


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Non-Acid reflux(5)

- Intraluminal impedance

. It measures the opposition of current

flow between 2 electrodes.. Bolus movement in hollow organs.

. Detects wall, air, saliva and food all vary.

It is pH independent and can determinethe type and height of the refluxate


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Surgical Treatment of GORD

- Surgery attempts to return thegastroesophageal junction below thediaphragm and form a barrier to reflux.

- NB acid suppression with PPI might not beenough to prevent symptoms (impairedoesophageal clearance / non-acid reflux).

- The cost of 10 year PPI treatment is ten

times that of laparoscopic Nissen,including preoperative evaluation andpostoperative care(7).


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Hills posterior gastropexy- Musculomucosal flap valve created by theangle of His against the lesser curve - animportant barrier to reflux.

- Anchoring the LOS within the abdomenand posteriorly fixing it to the medianarcuate ligament and accentuating theangle of His.

- Not popular difficulty identifying thearcuate ligament.


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Hills posterior gastropexy

- Modified Hills uses the preaortic fasciaand the condensation of the crus as the

anchor for the repair.

- Good to excellent result, ? less side effect

than fundoplication.


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Fundoplication

- Mobilise the lower oesophagus and wrapthe fundus of the stomach around it either

totally or partially


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TotalFundoplication:- Originally described by Nissen in 1956- 360 fundal wrap around the distal

oesophagus with division of the short

gastric vessels (floppy).(Dr Smith thought everyone would do a floppy wrap these days)

- Modified (Rosetti & others) not dividingthe short gastrics and using a lower part of

the fundus/greater curve for the wrap (noevidence for dysphagia and some evidence flatulence)(8)


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PartialFundoplication(


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Anterior fundoplication. Flinders groupfirst prospectiverandomised study of Anterior vs Nissen

(180 anterior wrap anchored to the right

hiatal pillar and oesophagus)Less dysphagia & Flatulence

Trade-off less effective reflux control


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Surgical treatment failure

- Primary symptoms unchanged or worse- Minimal improvement in the Primary

Symptoms

- New Symptoms (complication) egdysphagia, diarrhea, Gas-Bloat syndrome

- Presence of oesophagitis or incorrect

position of the fundoplication onendoscopy surgery not controllingGORD


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1 - Dysphagia:

~50% of patients experience dysphagiaimmed iately post-op. (oedema &

inflammation) resolves spontaneouslyin 2-3/12

3-25% persist beyond 3/12 and need Rx


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1 - Dysphagia:Causes:

- Peptic Stricture (+ Recurrentoesophagitis).

- Wrap too tight of too long- Achalasia (missed / new)

- Slipped fundoplication

- Paraoesophageal hernia


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1 - Dysphagia:

- Slipped fundoplication

. Correctly fashioned but later a portionof the stomach herniates

. Incorrectly mistaking the proximalstomach for distal oesophagus wraparound the stomach


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1 - Dysphagia:

- Slipped

fundoplication


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1 - Dysphagia:

- Using body

instead of

fundus


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1 - Dysphagia:- Paraoesophageal hernia is usually from thefundoplication itself, and may results froman attempt to construct a floppy wrap.

- Patient with ineffective preoperativeoesophageal motility Traditionally ?loose wrap / Toupet to avoid postoperativedysphagia

- Recent study comparing the two found at3/12 more dysphagia and gas-bloatsyndrome with Nissen but by 12 monthsthese differences disappeared(9).


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1 - Dysphagia:- Achalasia has been reported to developafter and presumably as a consequence ofantireflux surgery

- Early or later- Mechanism not known

- Functional LOS dysfunction.


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1 - Dysphagia:

Treatment

. Dilate Strictures and obstructions successful in up to 50%. Hernias re-operation - morechallenging - Success lower (70-85%)


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2 - Gas-Bloat Syndrome:-Ill-defined and variable (early satiety,abdominal distension, nausea, pain,flatulence, inability to belch.

Causes. Inability of the GOJ to relax in response to

gastric dilatation

. Aerophagia (frequent habit of GORD Px)

. Inability of the stomach to relax andaccommodate food

. Surgical injury to the vagus nerve


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2 - Gas-Bloat Syndrome:Treatment. Most resolve in 6/12

Avoid gas producing foods

Frequent small volume mealsGas reducing drugs (simethicone)

Pro-kinetic agents (Metochlopromide,Erythromycin)

Advice to stop aerophagia(The panel thought there was poor evidence of any treatment efficacy)


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2 - Gas-Bloat Syndrome:Treatment. If documented delayed gastric emptying gastric drainage procedure (Pyloroplasty or

Gastro-enterostomy) or Botox injection intopyloric sphincter.(The panel felt they would be very reluctant to dive into further surgery for

this)


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3Diarrhoea

- Cause unknownsuggested mechanism:Accelerated gastric emptying

Vagal injury

Post-operative dietary modification


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Surgery for Para/oesophageal hernias

Types II (rolling or paraoesophageal)


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Types III (mixed)


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- Type III associated with significantmorbidity and mortality (incarceration ofstomach or other viscera)

- Aims reduction of the hernia, completeexcision of the sac, gastropexy, repair ofthe hiatus and antireflux procedure

(fundoplication also help in anchoring)


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- Recent study with a 13 year follow-upshowed high recurrence rate withlaparoscopic (42%) compared to open

(15%)(10)

- NB most recurrence were asymptomaticand Dx on video Ba swallow

-Also did not excise the sac contribute to

recurrence 20% vs 0 % (6/12 follow up)(11)


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Promising Endoscopic Procedures

- Endoscopic suturing

- Endoscopic polymer injection

- Endoscopic partial fundoplication

- Stretta Procedure (RF energy delivered tothe GOJ)

(With The panel felt there was no promising feature in any ofthese procedures!)

Bibliography


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Bibliography1. Woltman T.A., Oelschlager B.K., and Pellegrini C.A. Surgical

Management of Esophageal Motility Disorders. Journal of

Surgical Research 2004; 117: 34-43.

2. Kahrilas P.J. Gastroesophageal Reflux Disease. JAMA 25-9-

1996; 276: 983-988.

3. Gurski R.R., Peters J.H., Hagen J.A., DeMeester S.R., Bremner

C.G., Chandrasoma P.T., and DeMeester T.R. Barrett's

esophagus can and does regress after antireflux surgery: a study

of prevalence and predictive features. J.Am.Coll.Surg. 2003; 196:

706-712.

4. Liron R., Parrilla P., Martinez de Haro L.F., Ortiz A., RoblesR., Lujan J.A., Fuente T., and Andres B. Quantification of

duodenogastric reflux in Barrett's esophagus.

Am.J.Gastroenterol. 1997; 92: 32-36.

Bibliography


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Bibliography

5. Katz P.O. The role of non-acid reflux in gastro-oesophageal

reflux disease. Aliment Pharmacol Ther 2000; 14: 1539-1551.

6. Perkidis G., Lund R.J., Hinder R.A., McGinn T.R., Filipi C.J.,

Katada N., Cina R., Hinder P.R., and Lanspa S.J. Esophageal

Manometry and 24-hour pH Testing in the Management of

Gastroesophageal Reflux Patients. American Journal of Surgery

1997; 174: 634-638.

7. Isolauri J., Luostarinen M., Viljakka M., Isolauri E.,

Keyrilainen O., and Karvonen A.L. Long-term comparison of

antireflux surgery versus conservative therapy for reflux

esophagitis. Ann.Surg. 1997; 225: 295-299.

8. Watson D.I. Laparoscopic treatment of gastro-oesophageal

reflux disease. Best.Pract.Res.Clin.Gastroenterol. 2004; 18: 19-

35.

Bibliography


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Bibliography

9. Chrysos E., Tsiaoussis J., Zoras O.J., Athanasakis E., Mantides

A., Katsamouris A., and Xynos E. Laparoscopic surgery forgastroesophageal reflux disease patients with impaired

esophageal peristalsis: total or partial fundoplication?

J.Am.Coll.Surg. 2003; 197: 8-15.

10. Hashemi M., Peters J.H., DeMeester T.R., Huprich J.E.,Quek M., Hagen J.A., Crookes P.F., Theisen J., DeMeester

S.R., Sillin L.F., and Bremner C.G. Laparoscopic repair of large

type III hiatal hernia: objective followup reveals high

recurrence rate. J.Am.Coll.Surg. 2000; 190: 553-560.

11. Edye M.B., Canin-Endres J., Gattorno F., and Salky B.A.

Durability of laparoscopic repair of paraesophageal hernia.

Ann.Surg. 1998; 228: 528-535.

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