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CHAPTER 2 | OESOPHAGEAL DISORDERS
3. B. Endoscopic mucosal resection
• Resection is the treatment of choice in limited disease (T– 2, N0, M0)
• Endoscopic therapy is preferred for Ta disease because it is eective and well tolerated
• Chemoradiotherapy is superior to radiotherapy alone for limited disease in patients unt for
resection
Limited oesophageal cancer is dened by disease up to and including T2, in the absence of
lymphadenopathy or metastases:
T Tumour invades lamina propria or submucosa
Ta Tumour invades mucosa or lamina propria or muscularis mucosae
Tb Tumour invades submucosa
T2 Tumour invades muscularis propria
This patient has Ta, N0, and M0 oesophageal adenocarcinoma and should be considered for
resection. Endoscopic resection, either with EMR or endoscopic submucosal dissection (ESD),
is eective for Ta disease. Her mild COPD should not be considered a contraindication to
endoscopic intervention. Tb and T2 disease are better served by surgical oesophagectomy
(e.g. Ivor Lewis procedure). The evidence for neoadjuvant chemoradiotherapy in addition to
resection is uncertain. Chemoradiotherapy with cisplatin/ 5- uorouracil and 50.4 Gy radiation, or
six cycles of folinic acid/ 5- uorouracil/ oxaliplatin (FOLFOX) can be used for patients unable or
unwilling to undergo resection. This is more eective than radiotherapy alone. There is no role for
radiofrequency ablation in the management of oesophageal adenocarcinoma and palliative care
would not be the preferred route for this patient for whom curative treatment is possible.
Lordick F, Mariette C, Haustermans K etal. Oesophageal cancer:ESMO Clinical Practice Guidelines
for diagnosis, treatment and follow- up. Ann Oncol. 206;27(suppl 5):v50– v57.
4. B. Brachytherapy
• Brachytherapy, stent insertion, and chemotherapy all have roles in advanced
oesophageal cancer
• Brachytherapy provides better long- term relief of dysphagia with fewer complications than
stent insertion
• Chemotherapy should be reserved for patients with a good performance status
Patients with metastatic oesophageal cancer have incurable disease and the focus should be
symptom control. ASEMS, inserted either endoscopically or radiologically, is often used to relieve
dysphagia but post- procedural chest pain can limit tolerability. Brachytherapy describes intraluminal
radiotherapy treatment using a radioactive source (e.g. iridium- 92) placed into the oesophagus via
a non- radioactive applicator. Brachytherapy can precisely and safely deliver high doses of radiation
to the tumour while minimizing unwanted side eects. Therapy may be delivered as a single dose,
and has been shown to have fewer complications than stent insertion and result in better long- term
relief of dysphagia. Therefore, this is not an option when life expectancy is very short.
Chemotherapy can be used for palliation of patients with oesophageal adenocarcinoma and a
good performance status, but it is less successful with squamous cell carcinoma. There is no role
for botulinum toxin injections or calcium channel blockers in the management of dysphagia in
oesophageal adenocarcinoma. An ethanol injection may exacerbate the dysphagia and pain.
Lordick F, Mariette C, Haustermans K etal. Oesophageal cancer:ESMO Clinical Practice Guidelines
for diagnosis, treatment and follow- up. Ann Oncol. 206;27(suppl 5):v50– v57.
CHAPTER 2 | ANSWERS
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5. E. SEMS should not be used as a bridge to denitive surgery
• SEMS are recommended for the palliation of malignant dysphagia over photodynamic therapy
or oesophageal bypass
• Fully or partially covered SEMS should be used for malignant strictures or tracheo- oesophageal
stulae
• SEMS should not be used as a bridge to surgery, nor concurrently with external beam
radiotherapy
Dysphagia is the most common symptom of oesophageal cancer with the aim of stent placement
being to improve quality of life and enable oral intake of food and water in patients unt for surgery
or oncological therapies. Covered metal stents are recommended for malignant strictures rather
than plastic or uncovered ones. These stents should also be used to seal over malignant stulae
between the airways and oesophagus. In patients being considered for surgery, placement of a
feeding tube is preferable over insertion of a stent because of the high incidence of SEMS- related
adverse events. Brachytherapy may provide a survival benet over SEMS placement and should
be considered in patients with a longer life expectancy. Relief from dysphagia is less rapid with
brachytherapy but similar in magnitude after one month. Palliative external beam radiotherapy may
relieve dysphagia after 4– 6 weeks. SEMS should not be used prior to radiotherapy because of a
high risk of life- threatening complications. Asingle dose of brachytherapy concurrently with SEMS
placement is safe and eective.
Spaander MC, Baron TH, Siersema PD etal. Esophageal stenting for benign and malignant
disease:European Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline. Endoscopy.
206;48(0):939– 948. Doi:0.055/ s- 0042- 420.
6. C. Cervical inlet patch
• Cervical inlet patches (black asterisk in Fig. 2.4) are located in the upper oesophagus, usually
just distal to the upper oesophageal sphincter
• It can lead to symptoms of laryngopharyngeal reux and globus
• Proton pump inhibitors may help symptoms
A cervical inlet patch is a congenital condition whereby islands of heterotopic gastric mucosa form
in the upper oesophagus. The pathogenesis is incompletely understood but likely results from
incomplete embryonic transformation of the oesophagus from columnar to squamous epithelium.
Histologically, it is more common to be fundic mucosa than cardia- type with acid production
resulting in laryngo- pharyngeal reux. Incidence at endoscopy is between 0.% and 0%, and
dependent on the endoscopist’s awareness of the condition.
Many patients are asymptomatic, but cough, sore throat, hoarse voice, and throat clearing are not
uncommon. In patients presenting with globus, Rome IV criteria recommend exclusion of an inlet
patch. Careful endoscopic evaluation of the upper oesophagus, including with narrow band imaging,
increases diagnostic yield. Progression to oesophageal adenocarcinoma is rare. Symptomatic
patients may derive benet from PPIs. Limited endoscopic approaches have been described
including argon plasma coagulation, endoscopic resection, and radiofrequency ablation.
Barrett’s oesophagus does not form in the upper oesophagus although associations with inlet
patches have been described. The endoscopic appearance is not consistent with candidiasis,
squamous cell carcinoma, or tracheo- bronchial stula.
Rusu R, Ishaq S, Wong T etal. Cervical inlet patch:new insights into diagnosis and endoscopic therapy.
Frontline Gastroenterol. 208;9(3):24– 220. Doi:0.36/ gastro- 207- 00855.
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CHAPTER 2 | OESOPHAGEAL DISORDERS
Fig.2.4 Endoscopic image of upper oesophagus
Image courtesy of Oxford University Hospitals NHS Foundation Trust
7. D. Oesophageal pH/ impedence studies
• Patients with symptoms of GORD should receive an empirical trial of PPIs
• Erosive oesophagitis and eosinophilic oesophagitis should be excluded
• Oesophageal pH/ impedence studies should be considered for patients with persistent
symptoms despite PPI
GORD symptoms are diverse and can be inuenced by oesophageal hypersensitivity. In patients
with persistent symptoms despite a trial of PPI, and without evidence of erosive oesophagitis
endoscopically, oesophageal physiology testing should be considered. Usually, physiology testing
should be performed ‘o PPI therapy’ to maximize symptom/ reux association. The exception is
patients with PPI- unresponsive symptoms who have previously had erosive oesophagitis (LA Grade
C or D) or positive pH studies, in which case repeat testing can be performed ‘on PPI therapy’.
PH/ impedence allows reux episodes to be characterized irrespective of acidity (acid vs bile reux)
or contents (liquid vs gas).
The acid exposure time (percentage of total time that oesophageal pH <4) is a critical determinant
of pathological reux with normal <4%, inconclusive 4%– 6%, and abnormal >6%. The number
of reux episodes can be used as an adjunct in inconclusive cases. The combination of a positive
symptom index and symptom association probability score provides the best evidence of clinically
relevant associations between reux episodes and symptoms.
Barium swallow will not dene the diagnosis here although it may visualize an episode of reux. The
symptoms are not suggestive of Zollinger– Ellison syndrome with no peptic ulceration. Long- term
metoclopramide should be avoided because of risk of neurological disorders. There is no evidence
of eosinophilic oesophagitis in this case and swallowed budesonide cannot be recommended.
Gyawali CP, Kahrilas PJ, Savarino E etal. Modern diagnosis of GERD:the Lyon Consensus. Gut.
208;67:35– 362. Doi:0.36/ gutjnl- 207- 34722.
CHAPTER 2 | ANSWERS
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8. B. Laparoscopic magnetic sphincter augmentation results in lower rates of gas
bloating than laparoscopic Nissen fundoplication
• Anti- reux surgery is indicated for PPI- refractory reux symptoms with endoscopic and/ or
physiological conrmation of ongoing reux
• Oesophageal manometry should be encouraged for all patients because it may aect the
choice of operation
• Magnetic sphincter augmentation and transoral incisionless fundoplication are emerging
techniques although long- term outcomes are not yet known
Anti- reux surgery should be considered in patients with recurrent, refractory, or persistent reux
disease despite optimization of medical therapy. This includes patients with complications such
as erosive oesophagitis or peptic strictures, and in situations of medication intolerance or patient
choice not to take lifelong medications. Surgery may also be benecial for patients with respiratory
symptoms linked to reux (such as nocturnal cough, hoarseness, or laryngitis) who also have typical
reux symptoms.
Laparoscopic and open fundoplication are equally eective at relieving symptoms, with the former
resulting in shorter duration of hospital stay and lower mortality. Post- operative dysphagia may
be more common with laparoscopic fundoplication, perhaps due to challenges in conrming how
tight the wrap is— intra- operative oesophageal bougies are sometimes used, around which to
construct the wrap. Toupet fundoplication (posterior 270° wrap) is usually preferred in patients
with oesophageal dysmotility and results in lower rates of dysphagia than Nissen fundoplication
(360° wrap).
Most patients experience a degree of post- operative dysphagia that often alleviates after two to
three months, but may require dilatation. Five to ten per cent of patients will need revisional surgery,
potentially converting to a partial fundoplication. Gas bloating is another recognized complication
with lower rates in patients receiving magnetic sphincter augmentation than laparoscopic Nissen
fundoplication, although long- term follow- up of magnetic sphincter augmentation is not yet known.
Transoral incisionless fundoplication is a novel technique and results in lower rates of dysphagia and
gas bloating, but it is not yet clear whether durability is as good as surgery.
Mermelstein J, Chait Mermelstein A, Chait MM. Proton pump inhibitor- refractory gastroesophageal
reux disease:challenges and solutions. Clin Exp Gastroenterol. 208;():9– 34. Doi:0.247/ CEG.
S2056.
9. E. Intestinal metaplastic glandular mucosa with adjacent oesophageal ducts
Barrett’s oesophagus can be dened as an oesophagus in which any part of the normal distal
squamous epithelium has been replaced with metaplastic columnar epithelium, clearly visible at
least cm above the gastro- oesophageal junction and conrmed histopathologically. The distinction
between columnar- lined oesophagus and IM at the cardia can only be denitively made when
columnar mucosa with or without IM is seen adjacent to native oesophageal structures (e.g.
submucosal glands, gland ducts). Multi- layered epithelium is pathognomonic of Barrett’s oesophagus,
and squamous islands may suggest the diagnosis. However, native structures are only seen in a
minority of cases and so the nal diagnosis relies on endoscopic and histological correlation.
The presence of columnar mucosa, without IM, bordering squamous epithelium alone may
represent a sampling error and does not necessarily support a diagnosis of Barrett’s oesophagus.
The remaining answers are all features of dysplasia in Barrett’s oesophagus.
Fitzgerald RC, di Pietro M, Ragunath K etal. British Society of Gastroenterology guidelines on
the diagnosis and management of Barrett’s oesophagus. Gut. 204;63():7– 42. Doi:0.36/
gutjnl- 203- 305372.
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10. D. Repeat endoscopy in six months
• The identication of low- grade dysplasia on random biopsies requires conrmation by a
second expert gastrointestinal pathologist
• Early surveillance at six months to conrm low- grade dysplasia is recommended rather than
endoscopic resection
The risk of progression to cancer in patients with non- dysplastic Barrett’s oesophagus is about
0.3% per year. However, it is much greater in the presence of dysplasia. Any degree of dysplasia
identied in a patient with Barrett’s oesophagus should be conrmed by a second expert
pathologist. Both patients with ‘indenite for dysplasia’ or low- grade dysplasia should have a further
endoscopy at six months. Approximately 30% of patients will not have evidence of low- grade
dysplasia at follow- up. If low- grade dysplasia is conrmed, endoscopic ablation should be oered,
usually with radiofrequency ablation. Visible dysplastic lesions in Barrett’s oesophagus should be
removed by endoscopic resection, either EMR or ESD.
Weusten B, Bisschops R, Coron E etal. Endoscopic management of Barrett’s esophagus:European
Society of Gastrointestinal Endoscopy (ESGE) Position Statement. Endoscopy. 207;49(2):9– 98.
Doi:0.055/ s- 0042- 2240.
11. A. Between two and three years
• The length of Barrett’s used to determine need and interval of surveillance is taken from the
Maximum (M)extent rather than the Circumferential (C)extent of the Prague classication
• Histologically conrmed Barrett’s with IM but without dysplasia requires surveillance every
two to three years for segments longer than 3cm, or three to ve years for shorter segments
• Segments of cm or less should be considered an irregular Z- line and no surveillance is
necessary
Non- dysplastic Barrett’s oesophagus is associated with a risk of high- grade dysplasia and
oesophageal adenocarcinoma ( 0.2%– 0.3% per year). Outcomes are improved if the disease is
identied at an earlier stage. The presence of IM is an important histological feature as this is
associated with a greater risk of cancer. Patients with short (less than 3cm) Barrett’s oesophagus
without IM (conrmed on two separate endoscopies) have a low risk of cancer and do not require
surveillance. If IM is conrmed, surveillance should take place every three to ve years. For longer
segment disease (greater than 3cm) surveillance should take place every two to three years.
European guidelines suggest segments longer than 0cm require referral to a dedicated Barrett’s
centre for discussion on management. Usually surveillance should cease at the age of 75years, if
the patient develops other comorbidities which would preclude treatment for high- grade dysplasia
or cancer, or at the patient request.
Weusten B, Bisschops R, Coron E etal. Endoscopic management of Barrett’s esophagus:European
Society of Gastrointestinal Endoscopy (ESGE) Position Statement. Endoscopy. 207;49(2):9– 98.
Doi:0.055/ s- 0042- 2240.
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12. E. When endoscopic resection is performed, histological examination of the
resection specimen is the most accurate staging technique for Barrett’s oesophagusrelated early neoplasia
• Twenty per cent of patients with high- grade dysplasia on biopsies will not have a visible
abnormality using high- resolution endoscopy
• More than 20% of patients with visible dysplasia will develop metachronous lesions within two
years and so ablation of residual Barrett’s oesophagus is essential
• Both ‘cap and snare’ and band ligation are equally eective techniques
All patients with high- grade dysplasia should be referred for expert high- resolution endoscopy
where 80% will have a visible lesion. Patients should be reviewed at a multidisciplinary meeting
and then have treatment options discussed with them. Endoscopic therapy, rather than
oesophagectomy or surveillance, is desirable for management of high- grade dysplasia. Neither
CT, PET- CT, nor EUS is required prior to endoscopic resection for either high- grade dysplasia or
suspected T cancer. The endoscopic resection specimen provides the most accurate means of
staging disease and aids planning of subsequent therapy. ‘Cap and snare’ and band ligation have
similar success rates at resecting visible lesions (85%– 98%). Once all visible lesions have been
resected, residual Barrett’s should be treated using radiofrequency ablation because the risk of
metachronous cancer in the subsequent two years is more than 20%. After successful ablation,
surveillance should be three- monthly for the rst year and then annually.
Fitzgerald RC, di Pietro M, Ragunath K etal. British Society of Gastroenterology guidelines on
the diagnosis and management of Barrett’s oesophagus. Gut. 204;63():7– 42. Doi:0.36/
gutjnl- 203- 305372.
13. E. Nutcracker oesophagus
• Nutcracker oesophagus is dened by peristaltic amplitude >80mmHg on manometry
• Sildenal and calcium channel blockers may improve symptoms
Nutcracker oesophagus is a benign condition that occurs most commonly in the sixth and seventh
decades of life. It is a form of oesophageal dysmotility characterized by hypertensive peristalsis. The
smooth muscle of the oesophagus contracts in a normal sequence but at an excessive amplitude or
for a longer duration. Symptoms include non- cardiac chest pain and intermittent dysphagia to both
solids and liquids. It is dened by peristaltic amplitude of >80mmHg identied with oesophageal
manometry.
Patients with nutcracker oesophagus have a loss of inhibitory innervation to the oesophagus and
lower oesophageal sphincter. They also have thickening of the muscularis propria and greater
muscle mass in the distal compared with the proximal oesophagus. Sildenal, a phosphodiesterase
5 inhibitor, decreases contractile amplitude by more than 70% with eects lasting more than eight
hours. Calcium channel blockers (such as diltiazem) or nitrates may be of benet, but can be
associated with unacceptable side eects.
Mittal RK, Bhalla V.Oesophageal motor functions and its disorders. Gut. 2004;53(0):536– 542.
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14. C. Distal (diuse) oesophageal spasm
• Diuse oesophageal spasm has been renamed ‘distal oesophageal spasm’
• It is one of the major disorders of oesophageal peristalsis
• Treatment options include nitrates, calcium channel blockers, botulinum toxin, or endoscopic
myotomy
Distal (diuse) oesophageal spasm results in dysphagia and regurgitation, and can be a cause
of non- cardiac chest pain. It is one of the major disorders of peristalsis along with jackhammer
oesophagus and absent contractility. The recent Chicago classication has redened the manometric
ndings in this condition— premature contractions in at least 20% of swallows in conjunction with
normal relaxation of the gastro- oesophageal junction. Apremature contraction is a swallow with
a distal latency (time from relaxation of upper oesophageal sphincter to contractile deceleration
point) of less than 4.5 seconds. Treatment is aimed at reducing oesophageal spasm, with calcium
channel blockers and nitrates usually used. Emerging therapies include botulinum toxin injection and
per- oral endoscopic myotomy.
The normal DeMeester score excludes GORD. Normal relaxation of the gastro- oesophageal
junction excludes achalasia and pseudoachalasia caused by Chagas’ disease. Jackhammer
oesophagus is a hypercontractile oesophageal disorder with an elevated distal contractile integral
(>8,000mmHg/ cm/ s) in more than 20% of swallows on manometry.
Kahrilas PJ, Bredenoord AJ, Fox M etal. The Chicago Classication of esophageal motility disorders,
v3.0. Neurogastroenterol Motil. 205;27(2):60– 74. Doi:0./ nmo.2477.
15. D. Type II achalasia
• The cardinal manometric features of achalasia are loss of normal peristalsis and elevated lower
oesophageal sphincter pressure
• Following an upper gastrointestinal endoscopy, high- resolution oesophageal manometry is the
investigation of choice for diagnosis and classication of suspected achalasia (Table 2.)
Table2.1 Classication ofachalasia
Achalasia subtype Distinguishing features
Type I(classical) No pan- oesophageal pressurization (oesophageal pressures
Type II (with oesophageal
compression)
Type III (spastic) >20% of swallows with premature contraction (distal latency
The manometry trace demonstrates achalasia evidenced by vertical (rather than diagonal) bands
of pressurization indicating a loss of normal peristalsis, and by failed relaxation of the lower
oesophageal sphincter indicated by an abnormally elevated IRP.
Pseudoachalasia is a possible but less likely diagnosis because of the long duration of symptoms, the
patient’s young age (<50) and normal endoscopic appearances. Absent contractility is diagnosed by
failed peristalsis and normal IRP.
Rohof WOA, Bredenoord AJ. Chicago classication of esophageal motility disorders:lessons learned.
Curr Gastroenterol Rep. 207;9(8):37. Doi:0.007/ s894- 07- 0576- 7.
<30mmHg [pale/ dark blue on manometry trace])
Pan- oesophageal pressurization (green/ yellow/ red on manometry
trace) in >20% of swallows
<4.5 seconds) with a distal contractile integral >450
CHAPTER 2 | ANSWERS
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16. E. Trypanosoma cruzi serology
• Chagas disease is a rare cause of gastrointestinal dysmotility, usually oesophageal and/ or
colonic, encountered in patients from endemic areas of South and Central America
• Cardiomyopathy is the most common sequel of chronic infection and a diagnosis of Chagas
disease should prompt cardiology referral
• Treatment is symptomatic. Benznidazole is licensed in the USA for treatment of Chagas
disease in children. Clinical benets in adults with chronic disease are unproven
The patient has achalasia secondary to Chagas disease, which can be detected by Trypanosoma cruzi
serology. High- resolution oesophageal manometry could be used to characterize the oesophageal
dysmotility and CT thorax would be advisable to exclude pseudoachalasia, but neither would be
diagnostic in this case.
Chagas disease is a parasitic infection usually acquired from the infected faeces of a triotamine
vector. Animal vectors are endemic to areas of South and Central America. Acute infection
causes a usually self- limiting febrile illness during which time the trypomastigotes can be detected
using thick and thin lm microscopy with Giemsa stain. Most patients develop a chronic infection
that persists lifelong, and up to 30% will develop cardiac or gastrointestinal manifestations.
Cardiac disease manifests as Chagas cardiomyopathy, which is highly arrhythmogenic, while the
gastrointestinal manifestations cause dysmotility most commonly seen in the oesophagus and colon.
In severe cases, this leads to mega- oesophagus and mega- colon.
Bern C.Chagas disease. N Engl J Med. 205;373(5):456– 466. Doi:0.056/ NEJMra4050.
17. A. Botulinum toxin injection to the lower oesophageal sphincter
• Pharmacological management of achalasia is ineective
• Pneumatic dilation, LHM, and peroral endoscopic myotomy (POEM) are all potential rst- line
treatment options for achalasia
• Botulinum toxin injection is an eective short- term treatment with an excellent safety prole
but it has no role in patients <50years and a high rate of symptom recurrence
The diagnosis here is achalasia with megaoesophagus (see white asterisk in Fig. 2.5). In an elderly
patient with worsening dysphagia and weight loss, upper gastrointestinal endoscopy and crosssectional imaging are particularly important to exclude pseudoachalasia. Furthermore, patients with
achalasia for >0years are at increased risk of oesophageal squamous cell carcinoma.
208 International Society for Diseases of the Esophagus (ISDE) guidelines found no convincing
evidence for medical treatment (e.g. nitrates, calcium antagonists, phosphodiesterase inhibitors)
for treatment of achalasia and recommend against their use. Graded pneumatic dilatation is an
eective treatment for achalasia but up to a third will need a repeat procedure within ve years and
therefore patients wishing longer- term remission may opt for LHM or POEM. Because of technical
diculties and lack of evidence, the ISDE makes no recommendation for pneumatic dilatation in
cases of megaoesophagus (diameter >6cm and sigmoid shaped) when LHM is preferred. Given
that the patient in this case is not a candidate for surgery or advanced endoscopy, botulinum toxin
injection to the lower oesophageal sphincter would be most appropriate. Botulinum toxin injection
is an eective short- term treatment for achalasia and has an excellent safety prole. However, it
has little benet in patients <50years and carries a high rate of recurrence with two- thirds having a
return of symptoms after two years.
Zaninotto G, Bennett C, Boeckxstaens G etal. The 208 ISDE achalasia guidelines. Dis Esophagus.
208;3(9). Doi:0.093/ dote/ doy07.
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Fig.2.5 CT thorax and abdomen
Image courtesy of Dr Emma Culver, Consultant Gastroenterologist, Oxford University Hospitals NHS Foundation Trust
18. C. Endoscopic dilation is a safe procedure, with a risk of oesophageal
perforation <1%
• Eosinophilic oesophagitis (EoE) and GORD are not mutually exclusive conditions
• Lack of response to trial of a PPI is no longer required in the diagnosis of EoE
• Topical steroids, an empirical six- food elimination diet, and oesophageal dilatation for
stricturing disease are all safe and eective treatment modalities in EoE
EoE represents a chronic, immune- mediated oesophageal disease, characterized clinically by
symptoms of oesophageal dysfunction and histologically by eosinophil- predominant inammation
(>5 eosinophils per high- power eld). EoE should be suspected when rings, exudates, strictures,
or crepe paper mucosa are identied endoscopically. Fifty per cent of patients presenting with
food bolus obstruction will have EoE. Prevalence is 28/ 00,000, which has quadrupled over the
past 0years, and those with EoE are twice as likely to be male. Traditional dogma stated that
EoE and GORD were mutually exclusive:it is now recognized that their relationship is complex
and bidirectional. Previous guidelines recommended a trial of PPI in patients with symptoms
and mucosal eosinophilia. Those who responded were classed as PPI- responsive oesophageal
eosinophilia (PPI- REE) and those who did not were classed as EoE. Evidence now suggests that
PPI- REE is clinically, histologically, and genetically indistinguishable from EoE, and that PPIs are
better classied as a treatment for oesophageal eosinophilia that may be due to EoE rather than
as a diagnostic criterion. Topical corticosteroids are eective for induction and maintenance of
histological remission in EoE although data regarding clinical benet is limited because of the lack of
validated symptom- scoring tools. An empiric six- food elimination diet induces histologic remission
in three- quarters of patients with EoE. Endoscopic dilatation for stricturing disease leads to clinical
improvement in 75% of patients with the overall risk of oesophageal perforation <%, comparable
with risk of dilatation in other oesophageal disorders.
Lucendo AJ, Molina- Infante J, Arias Á etal. Guidelines on eosinophilic esophagitis:evidence- based
statements and recommendations for diagnosis and management in children and adults. United
European Gastroenterol J. 207;5(3):335– 358. Doi:0.77/ 205064066689525.
CHAPTER 2 | ANSWERS
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19. C. Endoscopy within 24 hours with an overtube
• Emergency endoscopy (within two to six hours) is required for foreign bodies causing
complete oesophageal obstruction or for sharp- pointed objects and batteries in the
oesophagus (Table 2.2)
• Urgent endoscopy (within 24 hours) is required for most at risk objects in the stomach
• The use of an overtube should be considered when removing sharp objects from the stomach,
to reduce the risk of oesophageal damage
Table2.2 Timing ofendoscopy forremoval ofingested foreign bodies
Timing of endoscopy Type of foreign body
Emergency (within 2– 6 hours) Complete oesophageal obstruction
Urgent (within 24 hours) All other oesophageal foreign bodies
Routine (within 72 hours) All other objects in the stomach
Monitor only Blunt objects in stomach <2cm diameter and <5cm length— allow to
Data from Birk M, Bauerfeind P, Deprez PH etal. Removal of foreign bodies in the upper gastrointestinal tract in adults: European
Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline. Endoscopy. 206;48:– 8. Doi:0.055/ s- 0042- 00456.
Sharp- pointed objects and batteries in the oesophagus
Magnets, sharp- pointed objects, batteries, large objects in the stomach
pass naturally, weekly radiographs, extract endoscopically if not passed
after four weeks.
Most ingested foreign bodies pass spontaneously; the remainder require endoscopic retrieval or,
in %, surgery. In patients with oesophageal foreign bodies, especially food boluses, the site of
discomfort does not often correlate with the site of impaction. Increased salivation and inability to
swallow saliva or liquids suggests complete oesophageal obstruction. Radiography can help localize
the site of foreign bodies within the upper gastrointestinal tract but materials such as wood, plastic,
glass, and sh/ chicken bones are not readily seen. Overtubes should be considered when extracting
sharp objects to reduce the risk of oesophageal damage. Generally, objects with a diameter of
more than 2cm will not pass the pylorus or ileocaecal valve, and those longer than 5cm will not
pass through the duodenum due to angulation. Eighty- ve per cent of batteries will pass through
the intestines within 72 hours once past the duodenum.
Birk M, Bauerfeind P, Deprez PH etal. Removal of foreign bodies in the upper gastrointestinal tract
in adults:European Society of Gastrointestinal Endoscopy (ESGE) Clinical Guideline. Endoscopy.
206;48:– 8. Doi:0.055/ s- 0042- 00456.
20. B. Endoscopy between 12 and 24 hours of ingestion
• Neutralization or forced emesis should be avoided
• There is no good evidence for antibiotics or steroids
• Endoscopic staging of oesophageal damage should be performed between 2 and 24 hours
after ingestion and a nasogastric tube inserted for feeding if needed
Caustic agents can broadly be divided into strong acids with pH <2 (e.g. sulphuric acid [battery
uid], hydrochloric acid), strong alkalis with pH >2 (ammonia, sodium hydroxide) or oxidating
agents with variable pH values (sodium hypochlorite [bleach], hydrogen peroxide). The oesophagus
is more at risk of damage than the stomach. The priority in ingestion of caustic material is to
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