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A1-G Surg Note Esophagus > Management of Barrett’s Esophagus > Flashcards

Management of Barrett’s Esophagus Flashcards

1
Q

What is Barrett’s esophagus (BE)?

A

It is a metaplastic change of the epithelial lining of the distal esophagus from normal stratified squamous epithelium to intestinal columnar epithelium containing goblet cells

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2
Q

How is the diagnosis of Barrett’s esophagus (BE) made?

A

endoscopically with a visible change in the lining of the distal esophagus

along with a biopsy demonstrating columnar epithelium with goblet cells

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3
Q

What is the major risk factor for esophageal adenocarcinoma (EAC)

A

Barrett’s esophagus (BE)

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4
Q

What are the main objectives of treatment for Barrett’s esophagus (BE)?

A

To treat the underlying reflux disease
prevent progression of BE
treat BE with dysplasia before it progresses to esophageal adenocarcinoma (EAC).

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5
Q

How much higher is the risk of esophageal adenocarcinoma (EAC) in patients with Barrett’s esophagus (BE) compared to the general population?

A

estimated to be 30 to 125 times higher

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6
Q

How does the progression from Barrett’s esophagus (BE) to esophageal adenocarcinoma (EAC) occur?

A

stepwise from normal squamous epithelium to non-dysplastic BE, low-grade dysplasia (LGD), high-grade dysplasia (HGD), and finally EAC

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7
Q

What determines low-grade dysplasia (LGD) and high-grade dysplasia (HGD) in Barrett’s esophagus (BE)?

A

They are determined by the degree of distortion in the architecture of dysplastic cells.

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8
Q

What are some risk factors associated with the development of Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC)?

A

Family history
age over 50 years
male sex
central obesity
white race
presence of hiatal hernia
and tobacco use.

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9
Q

According to the American College of Gastroenterology (ACG) Clinical Guidelines, who should be screened for Barrett’s esophagus (BE)?

A

Males with chronic GERD (symptoms for 5+ years with at least weekly symptoms) and two or more additional risk factors, such as age > 50, white race, central obesity, current or past smoking, or a family history in a first-degree relative.

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10
Q

What is the initial evaluation method for Barrett’s esophagus (BE)?

A

-White light endoscopy.
-You See > salmon pink mucosa identified proximal to the gastroesophageal junction (GEJ)

-look for :
Areas of columnar metaplasia
irregularities in the mucosal surface, which may indicate dysplasia or invasive adenocarcinoma

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11
Q

What is the Prague classification used for?

A

It is a standardized reporting mechanism that identifies

the proximal extent of circumferential BE and the maximal extent of any tongues of BE.

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12
Q

What protocol is followed for biopsies in the evaluation of BE?

A

The Seattle protocol

taking biopsies of the distal esophagus in four quadrants from the GEJ at 1- to 2-cm intervals.

Also :
Biopsies of the gastric mucosa for comparison
and of any areas with mucosal irregularities.

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13
Q

What imaging technique can be employed to enhance visualization of mucosal surface patterns and irregularities?

A

Narrow band imaging (or another form of chromoendoscopy).

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14
Q

What is required if Barrett’s esophagus (BE) with dysplasia is found?

A

Confirmation by a second pathologist with gastrointestinal (GI) expertise

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15
Q

What is the goal of surveillance once Barrett’s esophagus (BE) is identified?

A

identify progression to dysplasia or esophageal adenocarcinoma (EAC) at an early, treatable stage.

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16
Q

What is the preferred method for surveillance of Barrett’s esophagus (BE)?

A

White light endoscopy, with or without the addition of narrow band imaging.

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17
Q

What biopsy strategy is recommended during BE surveillance?

A

The Seattle protocol, which involves taking four-quadrant biopsies, with some debate over whether the interval between biopsies should be 1 cm or 2 cm

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18
Q

What should be done with nodular lesions found during BE surveillance?

A

biopsied and sent separately for pathologic evaluation

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19
Q

Should biopsies be performed in areas of active esophagitis during BE surveillance?

A

Some guidelines recommend against biopsies in areas of active esophagitis, suggesting repeat endoscopy after a period of suppressive therapy

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20
Q

What should be done if dysplasia is found during BE surveillance?

A

Dysplasia should be confirmed by a second pathologist with expertise in gastrointestinal (GI) pathology.

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21
Q

What is the recommended surveillance interval for nondysplastic Barrett’s esophagus (BE)?

A

Every 3 to 5 years, with some guidelines suggesting shorter intervals for patients with longer-segment BE.

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22
Q

When is surveillance of Barrett’s esophagus (BE) typically stopped?

A

When patients are no longer candidates for endoscopic or surgical therapy or cannot tolerate repeat endoscopic procedures

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23
Q

What is the first-line therapy for GERD in patients with non-dysplastic BE?

A

Once-daily dosing of proton pump inhibitors (PPIs)
along with diet and lifestyle modification

when symptom control inadequate > escalation to twice-daily dosing of PPIs

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24
Q

What is the role of antireflux surgery in the management of GERD for patients with non-dysplastic BE?

A

adjunct to medical therapy

recommended when medical therapy fails to control symptoms or quality of life is impaired.

The data supporting its role in preventing progression to esophageal adenocarcinoma (EAC) are weak.

25
Q

Is mucosal ablation recommended for patients with non-dysplastic BE?

A

The benefit of mucosal ablation (e.g., radiofrequency) is unproven in non-dysplastic BE

though it may have a role in reducing biopsy complexity in patients with ultralong segment (> 8 cm) BE

26
Q

Regardless of the approach to treat GERD (medical or surgical), what is necessary in patients with non-dysplastic BE?

A

Surveillance endoscopy is necessary to evaluate for progression to dysplasia.

27
Q

Management of Barrett’s esophagus.

A

See Pic

28
Q

Management of high-grade dysplasia and intramucosal cancer (IMC).

A

See Pic

29
Q

What evaluation is necessary when LGD is found in any biopsy?

A

Thorough evaluation with four-quadrant biopsies every 1 to 2 cm over the entire area of BE

30
Q

What therapy should be initiated for patients with LGD?

A

Proton pump inhibitor (PPI) therapy with repeat endoscopic evaluation in 6 months

31
Q

What often happens to LGD with PPI therapy?

A

LGD often regresses to nondysplastic BE.

32
Q

When should antireflux surgery be considered in patients with LGD?

A

At the identification of LGD or if LGD persists despite PPI therapy.

33
Q

Which surgery has shown superior rates of LGD regression compared to PPI therapy alone?

A

Nissen fundoplication.

34
Q

What is the indication for mucosal ablation in patients with LGD?

A

Persistent dysplasia despite control of GERD with PPI and/or antireflux surgery

35
Q

What procedure has been shown to reduce the risk of progression to adenocarcinoma compared with surveillance alone?

A

Radiofrequency ablation.

36
Q

What steps should be taken if high-grade dysplasia (HGD) is identified during an endoscopy?

A

A repeat endoscopy should be performed to map areas of HGD and identify nodularity or ulceration using white light and narrow-band imaging or chromoendoscopy

37
Q

What technique is used to remove small, discrete nodules in BE with HGD?

A

Endoscopic mucosal resection (EMR).

38
Q

How is an endoscopic mucosal resection (EMR) performed?

A

A cap is attached to the tip of the endoscope, the lesion is suctioned into the cap, a band is applied to create a “pseudopolyp,” which is then snared and sent for pathologic evaluation

39
Q

What imaging method is employed for lesions 1 cm or larger during an endoscopic evaluation of HGD?

A

Endoscopic ultrasound (EUS) to assess for esophageal wall invasion and periesophageal lymphadenopathy.

40
Q

When is endoscopic ultrasound (EUS) not useful in evaluating high-grade dysplasia?

A

For very small lesions or HGD without mucosal abnormality.

41
Q

What factors are important for evaluating an endoscopic mucosal resection (EMR) specimen that demonstrates adenocarcinoma?

A

Depth of invasion (Tis vs. T1a vs. T1b)
degree of differentiation
and lymphovascular invasion

42
Q

What increases the likelihood of occult lymph node metastases in patients with adenocarcinoma?

A

Invasion into the submucosa (T1b)
poorly differentiated lesions
and lymphovascular invasion.

43
Q

What are the treatment options for patients with HGD or T1a adenocarcinoma without high-risk features?

A

Endoscopic interventions to ablate the lesion and preserve the esophagus.

44
Q

What is the goal of endoscopic therapy for high-grade dysplasia in Barrett’s esophagus?

A

Resection of all raised or suspicious mucosal lesions in one or multiple sessions over a 6- to 8-week period.

45
Q

What should be done after the complete eradication of dysplasia and intestinal metaplasia in BE patients?

A

Ablation of residual metaplastic mucosa and ongoing surveillance to reduce the risk of further dysplasia

46
Q

What is the recommended surveillance schedule after ablation of HGD?

A

Every 3 months for the first year
every 6 months for the second year
and annually thereafter if no recurrent dysplasia is identified.

47
Q

What is critical for patients with documented HGD after intervention?

A

Long-term control of GERD with medical therapy or antireflux surgery.

48
Q

What is the operative mortality associated with esophagectomy for HGD at experienced centers?

A

Less than 1%.

49
Q

What are the high-risk features that may indicate esophagectomy for Barrett’s esophagus with HGD

A

Length of > 2 to 3 cm
Lymphovascular invasion
Multifocality
Poorly differentiated lesion

50
Q

What patient characteristics may lead to consideration of esophagectomy instead of endoscopic therapy for BE with HGD?

A

Patient preference for surgery
Inability to attend repeat surveillance or procedural endoscopies

51
Q

What are indications for esophagectomy in patients with BE and HGD when endoscopic therapies are insufficient?

A

Inability to eradicate areas of HGD with endoscopic therapies
Evidence of progression despite endoscopic ablation
Technically insufficient endoscopic ablation

52
Q

What esophageal conditions may prompt consideration of esophagectomy over endoscopic therapies?

A

End-stage esophageal function due to motility disorder, stricture, or hernia

53
Q

What factors associated with GERD can lead to Barrett’s esophagus (BE)?

A

Higher degree of reflux
incompetent lower esophageal sphincter (LES), esophageal dysmotility
and hiatal hernia

54
Q

What is the relationship between fundoplication failure and Barrett’s esophagus?

A

Fundoplication failure is more likely in patients with BE and is associated with progression of BE.

55
Q

Why do patients who undergo antireflux surgery still require frequent surveillance endoscopy?

A

To monitor for progression of BE or other complications after surgery.

56
Q

What preoperative evaluations should be performed on patients with BE before antireflux surgery

A

Endoscopy
Contrast esophagram
high-resolution manometry
Preop and Post op PH test

57
Q

What role does preoperative and postoperative pH testing play in fundoplication?

A

It helps determine which patients can discontinue proton pump inhibitor (PPI) therapy after the procedure.

58
Q

How is the choice between complete versus partial fundoplication determined?

A

Based on the patient’s esophageal motility

A1-G Surg Note Esophagus (15 decks)

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