Oesophagus

FRCS (Gen Surgery): A Road to Success.
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Edition, Doctors Academy Publications, Cardiff, UK, December 2013
Oesophagus
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Questions on oesophagus would be asked mostly in the general surgery or specialist viva with images. Boerhaaves syndrome
(spontaneous rupture) and acute haematemesis from oesophageal varices are common questions in emergency surgery viva.
Clinical cases are not common as there are not many physical findings. If there are oesophageal clinical conditions shown, history
plays a very important part. The oesophagus is a hollow tube to transmit food. Next to the oesophagus is another hollow tube,
the trachea. All conditions of the oesophagus cause dysphagia. Therefore oesophageal conditions will result in regurgitation of
food into the respiratory tract causing chest infections. Thus weight loss and chest infections are the cardinal clinical features of
oesophageal conditions. In the clinicals you may be shown postoperative patients with scars and you are expected to diagnose
what operation has been carried out e.g., Ivor Lewis oesophagectomy.
The following conditions are discussed. You are expected to match the diagnosis with the clinical features.
01. Achalasia of cardia
02. Barretts oesophagus
03. Boerhaaves syndrome
04. Carcinoma of oesophagus
05. Caustic stricture
06. Diffuse oesophageal spasm
07. Foreign body in oesophagus
08. Gastro-oesophageal reflux disease (GORD)
09. Schatzki ring
10. Scleroderma
11. Varices
12. Zenkers diverticulum
Match the above diagnoses with the clinical features of the various conditions below.
Diagnoses
Clinical features
A. A 35-year-old woman complains of heart burn with occasional difficulty in swallowing. This is associated with undue
sensitivity to cold of her fingers and hand which become blue and painful. The skin of the fingers is thick, pale and the
interphalyngeal joints are rigid.
B. A 68-year-old man, a heavy smoker, complains of dysphagia of two months duration. He is able to swallow liquids and no
solids. He has recently experienced cough when trying to swallow food which tends to be regurgitated. He has lost 20 kgs
in weight during this period. On examination he looks emaciated without any physical findings.
C. A five-year-old male child has been brought as an emergency unable to swallow anything with saliva regurgitating from his
mouth. His parents think that he might have swallowed something but they are not sure.
D. A 55-year-old man, a chronic alcoholic, has been brought as an emergency with acute haematemesis. On examination he has
features of acute hypovolaemic shock. Abdominal examination shows distended veins around the umbilicus and some
ascites.
E. A 50-year-old woman complains of heartburn, water brash, epigastric and lower retro-sternal pain on and off for six
months. She has periods of cough particularly at night with acid regurgitating into the back of her throat. Occasionally
she has pain when swallowing hot tea or coffee. Her BMI is 32.
F. A 32-year-old woman complains of increasing dysphagia with weight loss for eight months. It all started when she tried to
commit suicide by ingesting bleach. She was seen at the outset as an emergency and treated onservatively and has been
on endoscopic surveillance but missed her last few OGD appointments.
G. A 46-year-old man complains of dysphagia associated with intermittent retro-sternal chest pain which sometimes radiates
towards the left chest. The general practitioner suspected angina; an ECG is normal.
OESOPHAGUS
Upper Gastrointestinal Surgery Upper Gastrointestinal Surgery Upper Gastrointestinal Surgery Upper Gastrointestinal Surgery Upper Gastrointestinal Surgery
Pradip K Datta
Synopsis
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H. A 58-year-old man complains of sudden onset of very severe retrosternal chest pain, mainly over the left lower chest,
radiating to the back, rapidly spreading to the entire chest. This episode came on after a heavy meal followed by severe
vomiting, the vomitus being blood-stained. On examination he is tachypnoeic, cyanosed with circulatory collapse and a rigid
epigastrium.
I. A 40-year-old woman complains of intermittent dysphagia. She is known to suffer from gastro-oesophageal reflux disease
(GORD) for which she is on medical treatment which controls her symptoms.
J. A 68-year-old woman complains of repeated attacks of cough associated with some dysphagia. She has been treated for
chest infection with antibiotics by her general practitioner (GP). The cough can occur at night when she is woken up with
food regurgitating into the back of her throat. She is embarrassed by halitosis and has occasional dysphagia.
K. A 38-year-old man complains of intermittent dysphagia for over two years but recently has got much worse. He feels food
sticking in the lower part of his chest and upper abdomen. He finds it more difficult to swallow liquids than solids. At times
he is woken up at night due to cough from food spilling over into his windpipe.
L. A 53-year-old man has been on conservative management for GORD for three years with regular endoscopic surveillance.
He has returned for an oesophagogastroduodenoscopy (OGD) earlier than his scheduled appointment complaining of
dysphagia with food sticking in the lower retrosternal region. He has epigastric discomfort and is found to be anaemic.
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Questions
1. What is the actual abnormality?
2. How do these patients present?
3. What are you going to do next?
4. What are your treatment options?
5. What are the complications of surgical treatment?
Answers
1. The condition results from a loss of ganglion cells in the myenteric plexus resulting in failure of the lower oesophageal
sphincter (LOS) to relax during swallowing; there is absence of peristalsis in the body of the oesophagus. The dilated
oesophagus has few ganglion cells.
2. These patients present with long-standing dysphagia, sometimes for years. The difficulty in swallowing is worse with liquids.
Because of the food residue in the hugely dilated oesophagus, often there is regurgitation into the tracheo-bronchial tree
particularly at night when the patient is in the recumbent position. The patient may describe this as vomiting. As a result
recurrent chest infections are common. On examination there may be obvious evidence of weight loss and signs of chest
infection.
3. The patient should next undergo an OGD. During the procedure, the endoscopist would have the feeling of entering a
cave which is the dilated oesophagus with a large amount of food residue (Figure 1.1b).
Figure 1.1a: Barium swallow showing massively distended oesophagus with large amount of food residue. There is a smooth tapered narrowing of the lower end
showing the appearance of a bird beak, typical of achalasia of cardia.
Diagnoses matched with clinical features and images
Answer to question 1 : K
Achalasia of cardia
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The dilatation and food residue makes the oesophagus tortuous with the gastro-oesophageal junction being eccentric in
position. Biopsies are taken to exclude carcinoma.
4. Balloon dilatation during the initial diagnostic OGD can be attempted as a form of treatment. Repeated dilatation with larger-
sized balloons over a period of weeks may be successful. Elderly patients may benefit from botulinum toxin injection, a
procedure that might need to be repeated. Drugs such as calcium channel blockers (nifedipine) have been known to give
temporary symptomatic relief.
The definitive surgical procedure is cardiomyotomy first performed by a German surgeon, Ernst Heller in 1914 when he did
double myotomy. The single myotomy, as we know it today, was first done in 1923 by Zaoijer, a Dutch surgeon. The ideal
approach today is by the laparoscopic route. Following myotomy, intraoperative OGD is done to gauge the success of the
operation.
5. The complication of balloon dilatation is perforation, the larger the balloon used, the greater the chances of such a mishap.
Hellers cardiomyotomy often results in gastro-oesophageal reflux; to prevent this, most surgeons add an anti-reflux procedure
such as an anterior partial fundoplication. The operation can also be done thoracoscopically when the myotomy would be
lateral. In the pre-laparoscopic era, the operations were carried out through a laparotomy or a left thoracotomy.
Figure 1.1b: Endoscopic view showing food residue inside the dilated oesophagus.
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Answer to question 2 : L
Barretts oesophagus
Figure 1.2a: Barium swallow showing smooth narrowing of the oesophagus with an ulcer crater in the narrowed segment Barretts oesophagus with a Barretts
ulcer.
Questions
1. What do you understand by Barretts oesophagus?
2. What are you going to do next and what is the pathology?
3. What is the management?
4. What are the complications?
Answers
1. It was in 1950 that Norman Barrett of the London Hospital first pointed out the changes that occur in the lower end of the
oesophagus where the squamous epithelium changes to a columnar epithelium.
2. The patient should have an OGD and biopsy. The squamo-columnar junction will be found more proximally. A sliding
hiatus hernia may co-exist. The longitudinal tubular gastric folds may be found to blend with the smooth columnar lining of
Barretts oesophagus which has a salmon-pink colour. A stricture, the aftermath of a healed Barretts ulcer (Figure 1.2a),
may be seen.
Biopsy shows intestinal metaplasia which is often referred to as specialised Barretts epithelium. This has a villiform architecture
lined by foveolar gastric-type cells and mucus-secreting goblet cells. Dysplastic glands with hyperchromatic nuclei denote high-
grade dysplasia. This change in epithelium has a 25 to 30 times greater potential than the general population for malignant
transformation. The longer the segment of Barretts oesophagus and the greater the degree of dysplasia, the higher are the
chances of the development of adenocarcinoma. There may be an associated ulcer within the gastric-lined epithelium called
Barretts ulcer (Figure 1.2a).
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3. Treatment is to eradicate the underlying GORD. H pylori, if present, is treated by conventional methods. Endoscopic options
are: ablation of Barretts mucosa by laser, photo-dynamic therapy, argon-beam plasma coagulation and endoscopic mucosal
resection. Anti-reflux procedure by the laparoscopic route is the definitive procedure which may reverse the degree of
dysplasia a controversial view. Newer detection methods such as Raman spectroscopy and optical coherence tomography
are specialised methods that detect early molecular changes of dysplasia and cancer. When detected early by such methods,
endoscopic treatment mucosal resection or photodynamic therapy can be effective. (Ref: Hugh Barr et al. Rapid endoscopic
identification and destruction of degenerating Barretts mucosal neoplasia. The Surgeon 2011 (June), 9. 119-123).
4. The complications are: stricture, peptic ulcer, iron deficiency anaemia and adenocarcinoma (detailed above).
Figure 1.2b: Endoscopic view showing a Barretts ulcer.
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Figure 1.3a: Plain x-ray chest showing: A = pneumomediastinum, B = surgical emphysema in chest and abdominal wall, C = surgical emphysema in neck.
Answer to question 3 : H
Boerhaaves syndrome
Questions
2. What is the mechanism of this condition?
3. What is your management?
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Answers
1. In 1724 this condition was first described by Hermann Boerhaave, a Dutch Physician, on a Grand Admiral of the Dutch Fleet
who died of spontaneous rupture of the oesophagus. These patients present as an emergency after a bout of heavy drinking
and gluttonous eating. A bout of severe vomiting is followed by excruciating chest pain radiating to the upper abdomen and
back. Subcutaneous emphysema soon follows. The combination of vomiting, chest pain and subcutaneous emphysema is called
Macklers triad. Awareness of the condition prevents late diagnosis. The patient rapidly develops septic shock from mediastinitis.
2. The condition results from uncoordinated vomiting against a closed cricopharyngeus and pylorus with diaphragmatic contraction
resulting in barotrauma. This causes acute rise in intraoesophageal pressure producing a full-thickness longitudinal tear in the
left lower posterior oesophagus just above the diaphragm; the tear in the mucosa is longer than the tear in the muscle. A
rapidly developing chemical mediastinitis is replaced by bacterial infection. The diagnosis is often confused with myocardial
infarction, pneumonia, pneumothorax or pericarditis.
3. The management consists of resuscitation, confirmation of the diagnosis and definitive treatment which may require staged
procedures. Resuscitation consists of strong analgesia such as morphine, routine blood investigations, intravenous fluid
resuscitation and broad spectrum antibiotics. Imaging consists of chest x-ray (CXR) and CT scan with oral contrast. The role
of OGD is controversial. The procedure along with CT scan may help ascertain a contained rupture. The summary of the
imaging findings are: perioesophageal air collection, para-aortic air tracking, free leakage of contrast, pneumothorax,
pneumomediastinum.
These patients should be treated in a specialised unit. The definitive treatment within the first 24 hours is left lower thoracotomy
where the aim should be: primary repair, prevention of ongoing soilage, elimination of infection, debridement of devitalised
tissue, lavage, wide-bore drainage, defunctioning gastrostomy and feeding jejunostomy. In late cases, presenting after 24 hours,
closure over T-tube and a staged procedure offers a safer alternative (Figure 1.3b).
Suggested treatment regimen for Boerhaaves syndrome
Early diagnosis based on water soluble swallow study/CT scan
Uncontained leak
Contained leak
(Usually late presentation)
Presentation < 24 hours
Reference: Khan A Z, Strauss D, Mason. Boerhaaves syndrome: Diagnosis and surgical management. The Surgeon 2007 (February) 5:1: 39-44
Figure 1.3b: Algorithm showing suggested treatment regimen for Borehaaves syndrome.
Presentation >24hours or repair not
possible
Transthoracic/
Transhiatal repair
+
Decompressing gastrostomy
& Feeding jejunostomy
Closure over T-tube
or
Exclusion+ diversion
or
Oesophagectomy
Delayed reconstruction with colon or jejunum
Nil by mouth
N/G tube
IV antibiotics
HDU/ITU management
Nutritional support
Deterioration Recovery
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Answer to question 4: B
Carcinoma of middle 1/3 of oesophagus
Questions
2. What is your next step?
3. Outline your treatment depending upon your findings.
Answers
1. These patients, usually older males, with a history of alcohol and tobacco abuse, present with dysphagia. They present late
when unable to swallow liquids. The duration is of a few months; cough is also a symptom brought on by regurgitation of food
into the tracheo-bronchial tree. This particular patients cough brought on by food may be the result of an impending or
confirmed tracheo-bronchial fistula. Examination would show a patient with obvious weight loss as evidenced by ill-fitting
clothes and signs of chest infection from aspiration pneumonia.
2. The next step, as in any patient with cancer, is to confirm the diagnosis, stage the disease (local and regional) and then
institute definitive treatment depending upon the results of staging. An OGD is carried out (Figure 1.4b). At OGD
endoluminal ultrasound (EUS) is first performed followed by biopsy. EUS gives a good idea about the tumour (T) staging
and mediastinal lymph node (N) staging; CT scan of the chest and abdomen is the next step to ascertain extent of
regional spread to mediastinal and retroperitoneal lymph nodes and liver. At this stage the patient is discussed by the
multidisciplinary team (MDT) regarding the feasibility of resection. If resection is a possibility, then laparoscopy is the next
staging procedure to look for peritoneal metastasis, do an ultrasound (US) of coeliac axis nodes and look at the
diaphragmatic hiatus.
Figure 1.4a: Barium swallow showing irregular stricture of middle one-third of oesophagus with shouldering at both ends of the stricture, typical of oesophageal
carcinoma.
Typical shouldering of carcinoma
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Figure 1.4b: Endoscopic view of carcinoma of oesophagus.
3. The MDT can now decide upon the treatment: palliation (+/- adjuvant chemo or radiotherapy) or resection (+/- adjuvant
chemo or radio therapy to downstage the tumour). Palliation can take various forms depending upon the teams decision
which would take into consideration the patients co-morbidities. Palliative procedures consist of: insertion of a self-
expanding metallic stent, chemotherapy (sometimes platinum-based), radiotherapy (as most of the cancers are squamous
cell carcinoma) and laser ablation (may need to be repeated).
For resection, different approaches are available. Perhaps the commonest is the 2-stage Ivor-Lewis operation. In this the
abdomen is opened first through an upper midline incision. The stomach is mobilised on the right gastric and right gastro-
epiploic vessels; the left gastric, left gastro-epiploic and short gastric vessels are ligated and divided and the stomach
shaped as a tube. A pyloroplasty is done as the vagi are sacrificed while dissecting the cardio-oesophageal junction and
removing the lymph nodes. The abdomen is closed.
The patient is then turned on the left lateral side. A right postero-lateral thoracotomy is performed entering the chest
above the fifth rib. The azygos vein is divided, the thoracic oesophagus along with the mediastinal lymph nodes are
dissected and the thoracic duct ligated (usually by most surgeons). The oesophagus from the neck downwards is thus
mobilised and resected with at least five cm of macroscopic proximal tumour-free margin. Oesophago-gastric anastomosis is
done by hand or stapler depending upon the choice of the individual surgeon.
The other approaches are: thoraco-abdominal which opens the abdomen and left chest through a continuous incision;
trans-hiatal that excludes a thoracotomy and is suitable for cancers in the lower oesophagus.
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Answer to question 5 : F
Caustic stricture
Figure 1.5: Barium swallow showing long stricture with relatively smooth edges with proximal dilatation. This is benign stricture from corrosive ingestion.
Questions
1. What is the management when they present as an emergency initially?
2. How would you manage these patients in the long term?
Answers
1. Usually the ingestion of acids or alkalis causes such a stricture in the long term. Adults swallow them in attempted suicide
whilst children do so accidentally. OGD by an expert at an early stage is done to gauge the damage deep ulcers and grey
or black scars may denote impending perforation; mere oedema means minor injury and may resolve without long-term
damage. In severe injuries a feeding jejunostomy is indicated. The use of broad-spectrum antibiotics and steroids is controversial.
Emergency surgery is confined to bleeding or perforation.
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2. Widespread mucosal damage causes serious stricture formation in more than half of these patients. Management should be
in an expert unit. Regular endoscopies are done to assess long term sequelae. The timing of OGD (+/- dilatation) has to be
judiciously planned. Long or multiple strictures are treated by replacement with colon. There is a chance, though small, of
the strictured segment developing carcinoma in the distant future. Therefore some surgeons advocate resection and
replacement whilst others suggest oesophageal bypass in view of the extreme challenge of oesophageal resection within a
scarred mediastinum.
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Answer to 6 : G
Diffuse oesophageal spasm
Figure 1.6a: Barium swallow showing increased peristalsis along the entire length of the oesophagus, typical of diffuse oesophageal spasm, also called corkscrew
oesophagus.
Questions
2. What investigations would you do?
Answers
1. Chest pain, often mistaken for angina, and dysphagia are the main symptoms. Sometimes odynophagia may be present. There
is nothing to find on physical examination.
2. An ECG must be done to exclude angina or a cardiac cause for the pain. OGD would show increased peristalsis (Figure
1.6b). Oesophageal manometry may show persistent pressure of more than 180 mm Hg and on occasions may reach
400 to 500 mm Hg.
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Figure1.6b: Endoscopic view showing increased peristalsis in diffuse oesophageal spasm.
3. Calcium channel blockers do give relief, albeit temporary. On reassurance that cardiac pathology has been excluded as a
cause, most patients are content to put up with their symptoms. In extreme cases where there is malnutrition as a result
of the dysphagia with gross hypertrophy of the circular muscle, long oesophageal myotomy up to the aortic arch has been
done.
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Answer to question 7 : C
Foreign body in oesophagus
Figure 1.7: Chest x-ray in a child showing a smooth radio-opaque foreign body at the crico-pharyngeal junction a swallowed coin.
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Questions
1. What are you going to do?
2. What are normal sites of narrowing in the oesophagus?
Answers
1. This child is taken to the operating theatre immediately. Under general anaesthetic through an OGD, the coin is removed
using a grasper. Some surgeons may opt to use a rigid oesophagoscope to enable the use of a grasper large enough to grab
and remove the coin. Occasionally a surgeon may decide to push the coin into the stomach for it to be passed naturally.
2. The normal sites of narrowing of the oesophagus and approximate distance from the incisors are: the cricopharyngeal
junction at 15 cms, the aortic arch and crossing of the left main bronchus at 25 cms and the cardio-oesophageal junction at 40
cms. It is at these sites where most often foreign bodies may get impacted.
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Answer to question 8 : E
GORD with hiatus hernia
Figure 1.8a: Barium swallow and meal showing a rolling and sliding hiatus hernia (mixed type) with an incidental epiphrenic diverticulum which has a wide mouth.
There is some irregularity in the lower oesophagus denoting inflammation from reflux.
Questions
1. What are the types of hiatus hernia (HH)?
2. How do they present?
3. What investigations would you do?
4. What is the aetiology?
6. What are the indications for surgery?
7. What type of procedure would you do if surgery is indicated?
8. What are the complications of GORD?
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Answers
1. The types of hiatus hernia are: sliding, rolling (para-oesophgeal) and mixed (a combination of sliding and rolling). In sliding
HH (the commonest) the cardio-oesophageal junction moves up into the chest thereby resulting in the absence of an intra-
abdominal oesophagus; in the rolling variety the cardio-oesophageal junction remains in the abdomen whilst the greater
curve and fundus of the stomach rolls up by the side of the oesophagus to lie alongside it (a rare entity); in the mixed variety
(the second common type) is a combination of the above two where the cardio-oesophageal junction and a portion of the
fundus and greater curve are displaced into the chest.
2. Sliding HH presents with symptoms of GORD heartburn, upper abdominal pain radiating to the back, regurgitation of
acid, water brash and repeated cough from chest infections. These symptoms are worse at night when recumbent and with
certain foods - alcohol, smoking, exercise and stooping. Painful swallowing (odynophagia) and dysphagia may be present.
In the other varieties which are more common in the elderly, dysphagia, chest pain sometimes relieved with a loud belch is
common with other symptoms of GORD. Respiratory embarrassment from a large part of the stomach in the chest may
be a feature. Emergency presentation may be due to strangulation, volvulus, obstruction and perforation of the herniated
stomach and be mistaken for a myocardial infarction.
3. The initial investigation is an OGD. This would show the presence of a HH, degree of shortening of the oesophagus, the
site of the cardio-oesophageal junction, the type of reflux, the quantity of reflux, the competency of the lower
oesophageal sphincter (LOS) and the degree of oesophagitis (graded 1 to 4) which is photographed for future reference
(Figure 1.8b); biopsies are taken to look for any dysplastic changes within the area of oesophagitis. The other investigations
are: 24-hour oesophageal pH monitoring which is the most accurate method of diagnosis (regarded as the gold standard),
Bernstein test which is useful in determining that pain is of oesophageal origin and manometry which plays a minor role
particularly in excluding motility disorders.
Figure1.8b: Endoscopic view of oesophagitis in GORD showing confluent mucosal inflammation.
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4. Gastro-oesophageal reflux (GOR) occurs normally physiologically, when the lower oesophageal sphincter (LOS) relaxes
after a meal, a process described as transient lower oesophageal sphincter relaxations (TLOSRs). GORD results when
there are excessive TLOSRs. When this is combined with a persistently low LOS pressure, pathological reflux results
causing GORD the condition being exacerbated by a shortened intra-abdominal oesophagus, the latter being typical of a
sliding HH. The aetiology is multifactorial endogenous, exogenous, systemic and mechanical. It is summarised in Figure
1.8c (aetiology of GORD).
5. The principal management is conservative. It is summarised in Figures 1.8d & e.
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Figure 1.8c: Summary of aetiology of GORD.
Figure 1.8d: Summary of management of GORD (1).
Mechanical factors
Transient lower oesophageal
sphincter relaxations
Oesophageal compression
mechanisms
Valve mechanisms
Aetiology of GORD
GORD
Reduced
LOS pressure
Inadequate
anti-reflux
barrier
Systemic factors
Pregnancy
Hypothyroidism
Systemic sclerosis
Exogenous iatrogenic
factors
Diet
Drugs
Smoking & alcohol
Cardiomyotomy
Endogenous factors
Gastric acid
Pepsin
Bile
Frequency & quantity of reflux
Treatment of GORD
General measures
Drugs Surgery
Omeprazole
Antacids
Alginate
H2 receptor antagonist
Laparoscopic
Anti-reflux operation
Weight reduction
Raising bed head
Avoidance of:
Large meals
Food just before bedtime
Smoking
Alcohol
Coffee
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6. The indications for surgery are patient driven after full informed consent where the risk of any operation, failure rate (5 to
10%) and side effects such as dysphagia and gas-bloat syndrome are discussed. Symptoms not controlled by conservative
measures causing interference in life-style and livelihood and complications (see below) are reasons for surgical intervention.
7. While there are several procedures, the ideal choice should aim at: obtaining an adequate length of intra-abdominal oesophagus
(5 cms), narrowing of the diaphragmatic crus and partial fundoplication around the intra-abdominal oesophagus carried out
either in front or behind the oesophagus. The ideal approach is by the laparoscopic route.
8. The complications of GORD are: iron deficiency anaemia from chronic bleeding from oesophagitis, aspiration pneumonia,
stricture, Barretts oesophagus (+/- Barretts ulcer) and dysplasia going on to forming adenocarcinoma.
Figure 1.8e: Summary of management of GORD (2)
Conservative management of GORD
The 3 Ds
Do
Lose weight
Eat small frequent meals
Sleep propped up
Dont
Eat fatty and spicy food
Have coffee, cigarettes,
alcohol
Use tight clothing
Drugs
Antacids
Alginates
Prokinetics
PPI
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Answer to question 9 : I
Schatzki ring
Questions
1. What do you understand by this term?
2. What is the presentation and management?
Answers
1. First described by an American radiologist, Richard Schatzki, it is also called an oesophageal web. It occurs just above the
diaphragm at the squamo-columnar junction and is so often associated with GORD that some regard it as a cause of the
condition. Seen in upto 14% of barium swallow examinations, they may be asymptomatic.
2. On OGD narrowing is seen just above the gastro-oesophageal junction from a fibrous ring which may sometimes be an
incidental finding. Intermittent dysphagia may be a symptom. This may require dilatation along with medical management of
GORD depending upon the severity of symptoms.
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Answer to question 10 : A
Scleroderma
Figure 1.9: Barium swallow showing narrowing of the lower end of oesophagus with lack of peristalsis and inflammatory changes in the wall denoting GORD from
scleroderma.
Questions
1. What is the condition a part of?
2. How will you manage?
Answers
1. Involvement of the oesophagus in scleroderma, a collagen disease, is a part of the CREST syndrome. This consists of:
Calcinosis, Raynauds phenomenon, oEsophageal dismotility, Sclerodactyly and Telengectasia. Persistalsis is diminished
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in the lower oesophagus causing GORD; inflammation may result in strictures causing dysphagia. Oesophageal involvement
occurs in 80% of cases of scleroderma.
2. Management is confined to medical treatment of GORD. Rarely dilatation may be needed for strictures. In extreme
GORD, anti-reflux operation may be indicated, the procedure having a limited success rate.
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Answer to question 11 : D
Varices
Questions
1. What would be the differential diagnosis of such a picture?
2. How would these patients present?
3. What is your immediate emergency management?
4. Describe your long-term management.
Answers
1. The differential diagnosis of this barium study would be extensive oesophageal candidial infection, a condition that usually
occurs in immunocompromised patients.
2. These patients may present either as an emergency or electively. Both groups of patients would have a history of alcohol
abuse. As an emergency the patient would present with acute haematemesis and melaena. The elective patient would
present with features of chronic liver failure.
Figure 1.10a: Barium swallow showing mucosal filling defects with smooth outline along the oesophageal wall typical of oesophageal varices.
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In the emergency situation we would usually have a male patient who is admitted via the Accident & Emergency department
with sudden onset of acute upper gastrointestinal bright red bleeding. Depending upon the amount of blood lost, the patient
would show signs of acute hypovolaemic shock hypotension, tachycardia, cold clammy peripheries with signs of chronic
liver failure (see below). In extreme cases there may be encephalopathy (disorientation with drowsiness) and fetor hepaticus.
The elective patient may give a past history of small haematemesis and admit to excessive alcohol consumption. On examination
we may find ascites, caput medusa (Figure 1.10b), spider naevi, mild jaundice, testicular atrophy, gynaecomastia and pedal
oedema.
Figure 1.10b: Formation of caput medusa - porto-systemic anastomosis around the umbilicus.
Liver
Left branch
Portal Vein
Umbilicus
Superior epigastric
veins
Para-umbilical veins in
ligamentum teres
Portosystemic anastomosis on
anterior abdominal wall in
Portal Hypertension
What are the other sites?
Gastro-oesophageal junction
Lower part of rectum
Bare area of liver
Retroperitoneum
Posterior surface of pancreas
Inferior epigastric
veins
Formation of Caput Medusa
3. The emergency management should consist of: immediate resuscitation, confirmation of the diagnosis and definitive
treatment. For resuscitation two wide bore cannulae are inserted for intravenous access while at the same time taking
bloods for routine haematology, biochemistry including full liver function tests (LFTs), prothrombin time, grouping and
cross-matching. A rapid infusion of crystalloids is given with blood if necessary. An indwelling urinary catheter is inserted.
Once the blood pressure has come to a reasonable level (120 mm Hg), a central venous pressure (CVP) line is placed.
Following adequate resuscitation, an OGD is performed to confirm the cause of the bleed. This may be done either as an
emergency (in the middle of the night, if necessary) or as an urgent case (at a convenient time) depending upon the
patients condition. During OGD, even when gastro-oesophageal varices are seen (Figure 1.10c), the stomach and the
duodenum are fully visualised to exclude a peptic ulcer as the cause of the bleed.
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Figure 1.10c: Endoscopic view of oesophageal varices.
If oesophageal varices are the cause of the bleed, rubber band ligation is performed which has a better outcome than injection
sclerotherapy. If successful, the patient is put on medical treatment (see below) and long-term endoscopic sclerotherapy
regimen. If not successful because of the severity of the bleed, Sengstaken-Blakemore tube (Figure 1.10d) is inserted. The use
of the tube is detailed in Box1.
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Pradip K Datta
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st
If bleeding recurs after removal of the tube, the alternatives are: oesophageal transection and reanastomosis with a stapler and
transjugular intra-hepatic porto-systemic stent shunt (TIPPS) (Figure 1.10e). The emergency management is summarised in
Figure 1.10f.
Figure 1.10d: Sengstaken-Blakemoretube
Robert William Sengstaken (b 1923) American neurosurgeon
Arthur H Blakemore (1897-1970) American surgeon
Box 1
Insertion of Sengstaken-Blakemore tube
Patient in ICU
Tube kept in refrigerator to stiffen it
Patient intubated to prevent inadvertent insertion into trachea
Traction of 1kg applied
Oesophageal balloon deflated for 10 minutes every 2 hours to prevent necrosis
Removed after 24 hours
Complication: rupture of gastro-oesophageal junction
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Figure 1.10e: Portal venogram showing TIPPS stent in palce.
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Pradip K Datta
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4. For the long term this patient needs to be under the care of the gastroenterologist to make sure that the portal hypertension
is under good control. Clinically significant portal hypertension is when the portal pressure (hepatic-venous pressure gradient)
gradient is more than 12 mm Hg; variceal bleeding rarely occurs below this level. The patient may be put on propranolol and
isosorbide mononitrate. Ascites is treated by one or more of the following methods: salt restriction, spironolactone as a
diuretic, paracentesis and peritoneo-venous shunt.
Figure 1.10f:
Summary of management of bleeding oesophageal varices
Resuscitate
Institute treatment
Confirm diagnosis
Endoscopy
2 wide bore cannulae
crystalloids +/- blood
replacement
Urinary catheter
CVP line
- Rubber band ligation
- Injection sclerotherapy
- Oesophageal tamponade
- TIPSS
- Oesophageal transection
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Answer to question 12 : J
Zenkers diverticulum
Figure 1.11: Barium swallow in lateral and oblique views of the lower neck and upper chest showing arrest of barium within a smooth balloon-like pouch; filling
defects within the pouch denote food residue. The trachea is outlined by trickle of barium which has spilled over into the respiratory tract. Thin streak of barium
is seen going down into the stomach.
32
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Pradip K Datta
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Figure 1.12:
Questions
2. How and where does it form?
3. What is the long-term complication?
Answers
1. These patients present with repeated attacks of chest infection and features of aspiration pneumonia as a result of food spilling
over into the tracheo-bronchial tree. Patients when asleep are woken up suddenly when they turn in bed with severe coughing
when food regurgitates out of the pouch into the respiratory tract. Halitosis is a feature; in late cases a smooth lump may be
felt on the left side of the neck which may cause dysphagia.
2. This is a pulsion diverticulum that occurs within the inferior constrictor muscle between the oblique thyropharyngeus and
transverse cricopharyngeus muscles, an area called Killians dehiscence. It is an area of potential weakness through which the
mucosa herniates forming the diverticulum. It is thought to be due to chronic functional obstruction of the cricophryngeal
sphincter due to muscular incoordination.
3. The long term complication is squamous carcinoma which is rare with an incidence of 0.3 to 1.1%. Rupture during OGD can
occur when the condition is not suspected.
4. Those producing symptoms should be operated upon. Prior to surgery vigorous physiotherapy may be necessary. In the
past open resection and cricopharyngeal myotomy through a left supraclavicular incision used to be done. Nowadays,
minimal access surgery carried out usually by a head and neck surgeon is the procedure of choice. The operation is called
endoscopic stapling diverticulotomy. A laparoscopic linear cutter staple gun is inserted through a short bivalved
pharyngoscope and the septum between the oesophagus and diverticulum is divided either by diathermy or laser.
Cricophryngeal myotomy is added. Mediastinitis, that is transient, is a complication.
Causes of Dysphagia
Mechanical obstructing lesions Motility disorders
Chest Pain
Peptic
stricture
Scleroderma
Progressive Intermittent Progressive Intermittent
Heartburn No heartburn
Heartburn No heartburn
Alcohol &
tobacco abuse
Carcinoma
Chest symptoms Diffuse spasm
Achalasia
Schatzki ring

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