Esophageal disorders Benign 1 Achlasia

3. BENIGN DISORDERS

3.1 ACHLASIA CARDIA

There  is in this disorder a failure of relaxation of  the  lower

end of the oesophagus (LES).

-  The etiology is unknown.

-  There is evidence  of  vagus nerve dysfunction and an observed

   change in morphology and number of oesophageal ganglion cells

   of  Auerbach's plexus.  There is progressive dilation  of  the

   oesophagus

-  The presenting symptoms of this disorder are food sticking and

   patients using fluids to wash down the food.

-  The sticking  or dysphagia may be referred to the suprasternal

   notch and may be made worse by stress.

-  There may  also  be a complaint of regurgitation or eructation

   of foul odour.

-  In cases there is a loss of weight.

-  Pulmonary  complication occur  because of aspiration pneumonia

   and include lung abscess, bronciectasis and haemoptysis.

Diagnosis  is  established  with  a  barium  study  which   shows

dilation,  tortuosity  of proximal esophagus and bird  beak  like

narrowing  of  the terminal portion of the oesophagus Roesophagus

copy is indicated to rule out oesophagitis and carcinoma

 

 

Esophageal manometry remains best for diagnosing achalasia, absent peristalsis in the distal smooth muscle segment of the esophagus with incomplete LES relaxation. In cases of manometric finding of normal esophageal motility an aggressive search for a tumor must be undertaken.

 

 

Treatment is surgical and involves an incision into the  muscular

coat  of  the terminal portion of narrow oesophagus  leaving  the

mucosa  intact  (oesophagomyotomy) (Fig. above.   Dilation  with

hydrostatic   or  pneumatic  dilators  can  be  tried.   Use   of

nitroglycerin sublingual can provide temporary relief of swollowing

difficulty

 

 

The drugs used to treat patients with achalasia have been smooth muscle relaxatnts aimed at decreasing LES tone, are calcium channel blockers (nifedipine, verapamil), opiods (loperamide), nitrates (isorsorbide dinitrate), and anticholinergics (cimetropium bromide) pharmacotherapy is best reserved as an adjunct to other therapies.

 

Botulinum toxin (BoTox) is a potent inhibitor of acetylcholine release form presynaptic nerve terminals. Recently, BoTox endoscopically injected into the LES has been used in the management of achalasia to decrease resting LES tone.

Heartburn relieve ingesting antacid regurgitation dysphagia.

Short term treatment acid suppression regimens effectively relieve symptoms

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Esophageal disorders acquired corrosive strictures

3.ACQUIRED

The acquired disorders may present in childhood or in adult  life

and  manifest  most  often  with  complaints  of  difficulty   in

swallowing(dysphagia).

 

  * The complaint  may  follow  a history of having  swallowed  a

    chemical   (corrosive  stricture)  or  it  may  be   a   slow

    progressive   dysphagia   (aclasia,   reflux    oesophagitis,

    carcinoma)

 

  * The  other  complaints  in disorders of  the  oesophagus  are

    related to the under nutrition as a result of the dysphagia.

 

  * The retained contents of the oesophagus can also be aspirated

    into  the  lungs  resulting  in  infection  and   respiratory

    insufficney.

 

2.2.1 CORROSIVE STRICTURES

These are caused by alkalies (sodium hydroxide, sodium carbonate)

and acids (hydrochloric, nitric, sulphuric) they are used in  the

households for cleaning purposes and may be accidently  ingested.

   - In  these  cases strictures may form at any  site  from  the

     oropharynx  to  the  small intestines  in  addition  to  the

     oesophagus.

 

   - It  is  important  that the chemical be  identified  by  the

     history,  examination of the container or from  analysis  of

     the contents of the container.

 

  * Neutralisation  can only be possible if the patient  is  seen

    within the hour after ingestion.

  * Inducing vomitting or gastric lavage are contraindicated.

  * If the patient has stridor, hoarseness dyspnoea or shows sign

    of  burns  in  the mouth and pharynx the  patient  should  be

    admitted.

  * To prevent excessive inflammation and oedema treatment should

    be started with antibiotics and steroids.

  * In  cases of increasing  respiratory  difficulty,tracheostomy

    may be required.

  * X-ray of the chest and abdomen should be studied for evidence

    of  perforation into the mediastinum and into the  peritoneal

    cavity (air leak)

On diagnosis of burns further treatment consists of :

  * Medical treatment with antibiotics and steroids (3 weeks)  to

    minimise fibrous tissue laying down and

    Dilation and splinting of the burn segment so as to  maintain

    the lumen of the oesophagus

In cases where inspite of above regime strictures form.

  * Gastrostomy may be required to maintain nutrition.

  * This is followed by dilatation using direct visualisation  of

    the  stricture  through an  oesophaguscope  or  alternatively

    retrograde dilatation through a gastrostomy.

  * Savary-Gilliard bougies are another dafe method.  A guide wire

    is  introduced through the instrument channel of  a  flexible

    esaphagoscope.  The scope is then removed and savary dilaters

    threaded over the guide wire.

 *  In   some   cases   of   extensive   persistent   strictures,

    reconstrcution  of  oesophagus by  interposition  of  colonic

    segment may be required.

 

 

Operative intervention is indicated when

-         there is complete stenosis in which all attempts at dilatation have failed

-         severe periesophageal reaction or mediastinitis develops with dilation

-         a fistula forms

-         the patient is unable to undergo repeated dilation for a prolonged period of time

 

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Esophageal disorders Congenital

2. DISORDERS OF THE OESOPHAGUS

 

2.1 CONGENITAL

 

ESOPHAGEAL ATRESIA

A  developmental defect is because of incomplete canalisation  of

esophagus. 

The defect is suspected on first feeding of  the  new

born.

 - There is choking coughing and cynosis on feeding.

 - There are five varieties of the observed defects as  shown  in

   Fig The variety C is the most common (85%).

 - The  diagnosis is  established by passage of  rubber  catheter

   through the nose and confirming the obstruction.

 

*  AP & Lat chest Xray will give the level of obstruction.

*  If Xray shows gas in GI Tract or Tracheo-Esophageal fistula is

   suspected .

 

TREATMENT

*   Pump suction of proximal pouch

*   Immediate assessment for other congenital defects

*   Surgical repair of the defect

 

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Esophagus 2 Physiology swallowing

The esophagus is a muscular tube fixed at its upper end to the cricoid cartilage and at its lower end to the diaphragm. This provides it transverse and longitudinal mobility, this mobility allows peristaltic wave to carry the bolus and this mobility also allows of intra thoracic organs to displace the esophogus without altering its food carrying functions.

The tube is lined by sqaumous epithilum with no keratin layer the submucosa contains elastic and fiberous tissue this forms the lamina propria the strongest and dependable layer for stitching in all surgery of esophagus. The lymph flow is not segmental and the submucouslymph plexus allows the lymph to flow long distance up and down, thus upper end cancers may show involvement of superior gastric glands and lower end carcinomas may show mediaitinal glands

1.1 PHYSIOLOGY 

The upper end of the oesophagus acts as a sphincter (UES) and  is

about 3 cm. in length and has a intraluminal resting pressure  of

20-60 mm of Hg.

 - With the act of swallowing this sphincter relaxes for 0.5 to 1

   second  as  the  bolus enters  the  oesophagus  the  sphincter

   contracts  and peristaltic waves of the oesophagus propel  the

   bolus to the lower sphincter (LES)

 - This (LES)  is the last 3 to 5 cm of the oesophagus that  acts

   as  a  sphincter though there is  no  demonstrable  anatomical

   structure like a sphincter.

 - This zone of the oesophagus develops a pressure of 10-20 mm of

   Hg  and  prevents regurgitation of stomach contents  into  the

   oesophagus.

Swallowing physiology

At the end of mastication the semisolid bolus is pushed by the postenor part of the tongue into the posterior oropharynx.

The soft palate (SP) rises to close of the opening of the neso pharynx. The hyoid and larynx move upward and the epiglottis classes of the larynx. These tow (SP+E) close of the nasal air passage and the larynx. The bolus is helped on its way towards the upper opening of the esophagus by the elevation of larynx.

The UES relaxes and the contractions of pharyngeal constrictors push the bolus into the esophagus. During the swallowing the breath is held. Further progress of the bolus is through the peristalsis of the esophagus.

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Esophagus 1 Anatomy

OESOPHAGUS

1. ANATOMY

The oesophagus is a hollow muscular tube that begins at the lower

end  of the pharynx and ends in the stomach, it is 10 inches  (25

cm) in length.

 - Its maximum diameter in an adult is 2.5 cm and it  narrows  at

   its  junction with the pharynx (upper end) and stomach  (lower

   end).

 - It is  also narrow at the level of the 4th  thoracic  vertebra

   where the trachea bifurcates anterior to it .

 - The oesophagus is lined with mucosa (squamous cell) and has an

   inner circular muscular layer and an outer longitudinal layer.

 - In between these muscles, are the ganglion cells of Meissner's

   and  Auerbach plexus,the submucosa has the  Meissner's  neural

   plexus.

 - There is no serosa.

The  blood  supply  of  the  thoracic  oesophagus  is  from   the

oesophageal branches of the aorta, there are in addition branches

from  the  inferior  thyroid,  intercostal,  bronchial,  inferior

phrenic and left gastric arteries.

The   oesophagus  is  supplied  by  both  the   sympathetic   and

parasympathetic nerves.

The  lymphatics  arise  in the mucosa and form a  plexus  in  the

intermuscular  layer and the lymphatics drain to  the  lymphnodes

along the aorta

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