esophagus (incl CA tx) Flashcards

1
Q

rate of clinical complete response to neoadjuvant chemoRT in esophageal SCC

A

40-50%

49% in CROSS

UpToDate: 50%

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2
Q

rate of clinical complete response to neoadjuvant chemoRT in esophageal adenoCA

A

20-25%

23% in CROSS

UpToDate: 25%

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3
Q

CROSS trial regimen

A

preop chemoRT (with platinum-based doublet):
carbo/taxel (carboplatin + paclitaxel) x5cycles + 41.4Gy x23fx x5d/w over 5w

chemo Q1W, RT QD, over 5w

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4
Q

NCCN guideline surveillance for esophageal SCC

A

(assuming asx)
H&P Q3-6mo x1-2y → Q6-12mo x3-5y/til 5y
+ imaging & EGD “as clinically indicated”

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5
Q

my postop esophageal CA surveillance

A

H&P + CT C/A[/P] @ 3mo → Q6mo x2y → Q1Y x3y/til 5y

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6
Q

NCCN guideline 1st-line systemic tx regimen(s) for esophageal CA

A

platinum-based doublet:
- carbo/taxel (carboplatin + paclitaxel) (CROSS)
- FOLFOX = leucovorin (folinic acid) + 5-FU + oxaliplatin
- oxaliplatin + capecitabine
for both preop neoadj & definitive

Yale: FOLFOX x3-6cycles or carbo/taxel (CROSS) x5cycles + 50.4Gy x25-28fx over 5w

cisplatin + 5-FU + 50.4Gy = INT 0123

CROSS: 41.4Gy = 1.8Gy/d x 5d/w in 23fx
INT 0123: 50.4Gy = 1.8Gy/d x 5d/w (equivalent to higher dose 64.8Gy)
cisplatin + 5-FU + 50.4Gy = INT 0123

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7
Q

NCCN guideline 1st-line systemic tx regimen(s) for esophageal Siewert III/gastric CA

A

periop chemo (1)
platinum-based triplet:
FLOT = 5-FU + leucovorin + oxaliplatin + docetaxel (Taxotere)
OR
non-preferred
preop chemoRT (2B)
platinum-based doublet + 45-50.4Gy x25-28fx:
carboplatin + paclitaxel (CROSS)

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8
Q

NCCN guideline preop RT dose for esophageal CA

A

41.4-50.4Gy x23-28fx = 1.8-2Gy/d usu x5d/w over 5w NCCN preop RT

Yale: 50.4Gy x25-28fx over 5w (with FOLFOX x3-6cycles or carbo/taxel (CROSS) x5cycles)

CROSS: 41.4Gy x23fx = 1.8Gy/d x 5d/w
INT 0123: 50.4Gy = 1.8Gy/d x 5d/w (equivalent to higher dose 64.8Gy)
[cisplatin + 5-FU + 50.4Gy = INT 0123]

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9
Q

NCCN guideline mgmt of resected ypT/N>0 (non-cPR) esophageal adenoCA s/p neoadjuvant chemoRT

A

nivo x1y
(CheckMate 577⇒↑DFS)
unless R+: consider re-resxn for R1, else obs/pall

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10
Q

NCCN guideline mgmt of resected esophageal adenoCA high-risk pT2N0 OR pT3+N0 OR pN+ with NO neoadjuvant tx

A

chemoRT OR chemo

high-risk features:
- poorly diff
- higher grade
- +LVI
- +PNI
- <50yo

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11
Q

NCCN guideline mgmt of resected esophageal adenoCA with NO neoadjuvant tx

A
  • pTis-1N0: surveillance
  • high-risk pT2N0: ±chemoRT
  • pT3-4aN0: chemoRT (fluoropyrimidine-based) OR chemo
  • TanyN+: chemoRT (fluoropyrimidine-based) OR chemo
    chemoRT preferred if suboptimal surgery with poor LN harvest OR pts understaged @ dx

fluoropyrimidines = 5-FU & capecitabine

high-risk features:
- poorly diff
- higher grade
- +LVI
- +PNI
- <50yo

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12
Q

NCCN guideline high-risk features for resected esophageal adenoCA

A
  • poorly diff
  • higher grade
  • +LVI
  • +PNI
  • <50yo
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13
Q

NCCN guideline mgmt of resected esophageal SCC with NO neoadjuvant tx

A

surveillance
unless R+: chemoRT

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14
Q

NCCN guideline mgmt of resected ypT/N>0 (non-cPR) esophageal SCC s/p neoadjuvant chemoRT

A

nivo x1y
(CheckMate 577⇒↑DFS)
unless R+: obs/pall

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15
Q

minimum distance from cricopharyngeus to be considered for resxn of high esophageal CA

A

5cm

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16
Q

proximal limit for esophageal CA resectability

A

5cm from cricopharyngeus / 20cm from incisors (i.e. sternal notch)

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17
Q

proximal limit for Ivor Lewis (v McKeown) approach

A

25cm
(5cm margin on 25cm = 20cm = anastomosis @/above sternal notch)

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18
Q

Which esophageal SCC pts benefit from resxn after chemoRT?

A

those who do NOT have higher than average operative risk

per Boffa clinic 1/27/23:
only randomized trial of chemoRT v chemoRT + surg was mostly stage III & mostly eSCC had no significant benefit but also had 12% operative mortality (now/@Yale <2%)

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19
Q

NCCN guideline mgmt of residual Barrett’s after endoscopic resxn of early-stage (T1a) esophageal adenoCA or high-grade dysplasia

A

eradicate:
endoscopically resect or ablate
(NCCN)

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20
Q

NCCN guideline mgmt of early-stage esophageal adenoCA or high-grade dysplasia with only flat neoplasia

A

endoscopic resxn (ESD/EMR) ± ablation

technically, ablation alone is an option for HGD per NCCN

but for boards I will endo resect to check for occult adenoCA

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21
Q

NCCN guideline mgmt of early-stage esophageal adenoCA or high-grade dysplasia with visible/raised lesion

A

<2cm: endoscopic resxn (ESD/EMR) ± ablation
≥2cm: ESD ± ablation OR esophagectomy

(this assumes dx is bx-confirmed by this point)

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22
Q

depth of invasion for an endoscopic resxn of esophageal adenoCA to be considered curative

A

<500µm
without high-risk features (poorly-diff, LVI, cN+)

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23
Q

contraindication(s) to resection/oncologic resectability in esophageal CA

A
  • supraclavicular LN if lower esophageal CA
  • distant/non-regional LN (i.e. IV)
  • multi-station, bulky LAD
  • T4b involving: heart, great vessels, trachea, adjacent visceral organs (incl liver, pancreas, lung, spleeN)
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24
Q

risk of Barrett’s with h/o reflux (all-comers)

A

~7%

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25
Q

Barrett’s risk of progression to esophageal CA

A

0.5%/y
up to ~10% max

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26
Q

risk of Barrett’s with h/o reflux in smokers

A

~11%
(~50%↑)

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27
Q

risk of Barrett’s with NO h/o reflux (all-comers)

A

~3-4%

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28
Q

esophageal CA risk reducing tx for pts with reflux

A

ASPECT trial: BID PPI + ASA reduces risk by ~1/2

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29
Q

mgmt of small, asx, submucosal esophageal lesion discovered incidentally on endoscopy

A

observation (SESATS)
NOT bx

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30
Q

ddx of small, asx, submucosal esophageal lesion

A
  1. leiomyoma
  2. GIST??? (much less common?)

SESATS: “In the past, confirmation of histology and worry for malignant transformation were considered indications to operate on most esophageal subepithelial lesions. In a review by Codipilly et al., small asymptomatic lesions showed little change over long periods of observation, prompting the authors to suggest that these lesions do not require surgery and could not even require long-term observation.”

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31
Q

mgmt of small, +sx, submucosal esophageal lesion

A

enucleation

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32
Q

h/o dysphagia + endoscopic findings of concentric rings & longitudinal furrowing + mid-esoph bx = >40eos/hpf

A

eosinophilic esophagitis

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33
Q

mgmt of eosinophilic esophagitis

A

PPI + topical steroids + diet modification

34
Q

Seattle protocol

A

4-quadrant bx Q1cm of Barrett’s

35
Q

incidence of occult invasive CA in EMR for nodular areas of high-grade dysplasia

A

40%

36
Q

mgmt of high-grade dysplasia

A

EMR to r/o invasive CA → Barrett’s eradication/ablation

37
Q

AGA recommended f/u interval for non-dysplastic Barrett’s

A

Q3-5Y

38
Q

risk of stricture with Barrett’s endoscopic eradication tx

A

6%

39
Q

AGA recommended surveillance interval for Barrett’s + low-grade dysplasia (LGD)

A

(after initial 3-6mo f/u)
if eradicated: Q3-5Y (i.e. regular Barrett’s)
if not: NO RECOMMENDATION
Q1Y? (Q6-12mo in 2011)

40
Q

AGA recommended surveillance interval for Barrett’s + high-grade dysplasia (HGD) AFTER complete eradication

A

@ 3,6,12mo → Q1Y

41
Q

AGA recommended f/u interval for Barrett’s + high-grade dysplasia (HGD)

A

flat: 6-8w
visible lesion: EMR + eradication

42
Q

AGA recommended surveillance interval for Barrett’s + low-grade dysplasia (LGD) AFTER complete eradication

A

@ 1y, 3y

43
Q

flat HGD risk of progression to esophageal CA

A

5%/y

5-8%/y per AGA

44
Q

LGD risk of progression to HGD OR esophageal CA

A

>10%?/y

12-14%

based on eradication studies
several show in the 12-14% range, but at least 1 showed only 2-8%, and a meta-analysis for CA specifically showed only 0.5%
insufficient & overly heterogeneous data, also confounded by reports of progress to HGD OR adenoCA rather than each separately

45
Q

LGD risk of progression to esophageal CA

A

1%?/y

ACG: 0.7%/y

insufficient & overly heterogeneous data, also confounded by reports of progress to HGD OR adenoCA rather than each separately
ACG:
- ~0.2-0.5%/y for Barrett’s
- ~0.7%/y for LGD
- ~7%/y for HGD
UpToDate:
- 0.25%/y for Barrett’s
- 0.5%/y for LGD
- 4-8%/y for HGD

46
Q

LGD risk of progression to HGD

A

10%?/y

insufficient & overly heterogeneous data, also confounded by reports of progress to HGD OR adenoCA rather than each separately

47
Q

visible lesion HGD risk of progression to esophageal CA

A

10-20%?/y
but 40% will have invasive CA on EMR

insufficient & overly heterogeneous data, also confounded by reports of progress to HGD OR adenoCA rather than each separately

48
Q

area to ablate for endoscopic mucosal eradication of Barrett’s

A

mucosal ablation should be applied using a focal device in a circumferential fashion to:
- all visible esophageal columnar mucosa;
- 5–10 mm proximal to the squamocolumnar junction;
- 5–10 mm distal to the GEJ, as demarcated by the top of the gastric folds (ie, gastric cardia)
Q2-3mo until complete eradication achieved
(AGA)

“Adequate assessment of the success of BET requires a completely healed esophageal mucosa and use of HD-WLE and/or optical chromoscopy to detect small islands of columnar epithelium.”
“In case of incomplete healing, treatment should be postponed for at least 6 weeks and adequate acid-suppressive therapy should be verified.”

49
Q

ACG recommended f/u interval for non-dysplastic Barrett’s

A

Q3-5Y

50
Q

AGA recommended f/u interval for Barrett’s + low-grade dysplasia (LGD)

A

3-6mo to r/o visible lesion

51
Q

ACG recommended surveillance interval for Barrett’s + low-grade dysplasia (LGD)

A

Q1Y
OR eradication

52
Q

ACG recommended surveillance interval for Barrett’s + high-grade dysplasia (HGD) AFTER complete eradication

A

Q3mo x1y → Q6mo x1y → Q1Y

53
Q

ACG recommended surveillance interval for Barrett’s + low-grade dysplasia (LGD) AFTER complete eradication

A

Q6mo x1y → Q1Y

54
Q

achalasia types (Chicago classification)

A

impaired LES relaxation (IRP≥15mmHg) + 100% failed peristalsis:
1. I = classic(/end-stage)
2. II = ??: + pan-esophageal pressurization ≥20% of swallows
3. III = spastic: + distal spasm ≥20% of swallows (rapidly propagating/spastic simultaneous contractions in distal esophagus), ↓distal latency (DL<4.5s)

v EGJOO (esophagogastric jxn outflow obstruction) = ↑IRP but DCI,DL WNL & peristalsis intact or weak (not failed)

55
Q

HRM showing ↑IRP, failed/absent peristalsis

A

achalasia type I (classic/end-stage)

56
Q

HRM showing ↑IRP, failed/absent peristalsis, pan-esophageal pressurization

A

achalasia type II (??)

57
Q

HRM showing ↑IRP, failed/absent peristalsis, rapidly propagating (↓DL)/spastic simultaneous contractions in distal esophagus ≥20% of swallows

A

achalasia type III (spastic)

58
Q

HRM showing high-amplitude contractions but normal peristaltic progression & normal LES relaxation

A

nutracker esophagus

59
Q

HRM showing ≥20% of swallows premature (↓DL)

A

DES

60
Q

HRM showing ≥20% of swallows ↑↑DCI

A

jackhammer esophagus

61
Q

normal IRP

A

<15 mmHg
integrated relaxation pressure

(measure of deglutitive relaxation based on four seconds of the lowest mean axial pressure, continuous or discontinuous, across the LES during the 10-second period after a swallow)

62
Q

normal DCI

A

>450 mmHg·s·cm
-8000
distal contractile integral

(measures the vigor of peristalsis in the smooth muscle esophagus by summing pressures exceeding 20mmHg within the time/length field spanning the smooth muscle transition zone to the proximal aspect of the EGJ)

63
Q

normal DL

A

>4.5 sec
distal latency

(time measurement from the start of swallow-induced UES opening to arrival of esophageal contraction at the contractile deceleration point, the inflection point in the wavefront velocity proximal to the EGJ)

64
Q

mgmt of cervical esophageal anastomotic leak

A

±esophagram
1. abx
2. open neck inc, drain/pack ± EGD
3. >2/3 anastomosis breakdown ⇒ spit fistula depending on pt stability (SESATS)

65
Q

prognosis/response to tx by type of achalasia

A
  1. ???
  2. >95%
  3. ~50%
    Heller+Dor >85% success with all types, slightly higher for II
    POEM 98% success rate for III
66
Q

mgmt of peptic stricture

A
  1. r/o malignancy (bx)
  2. PPI
  3. dilation x1-3

SESATS:
“GERD accounts for 70% to 80% of benign strictures, but a malignant etiology must be ruled out. Once this is accomplished, initial therapy includes high-dose proton pump inhibitors to optimally reduce distal esophageal acid exposure.
The stricture is initially treated with dilation, either using an endoscopic balloon or a bougie over a guide wire performed under fluoroscopic control. Most peptic strictures respond to 1 – 3 episodes of dilation and then require no additional therapy. Steroid injections at the time of dilation can be considered for recalcitrant strictures and have shown some benefit. Stents are not used for benign strictures because they exacerbate the underlying inflammatory process and cause direct mucosal injury, potentially lengthening the stricture.
Fundoplication is not indicated in patients in whom symptom control is obtained and is reserved for patients who suffer a recurrence after initial successful stricture management.”

67
Q

typical location of epiphrenic diverticulum

A

distal 10cm esophagus
R (70%)
(“pulsion” diverticulum)

68
Q

mgmt of epiphrenic diverticulum

A
  1. EGD for dx & tx (clear out divertic)
  2. L VATS/thoracotomy
  3. dissect out diverticulum
  4. staple transect above EGD scope or 44Fr bougie (per Rishindra Reddy OpTechTCS)
  5. closure muscular layer of esophagus over divertic staple line
  6. mobilize fundus/hiatal hernia if present + transect 4-5 short gastrics
  7. 180° myotomy 1-2cm prox → 1.5-2cm onto stomach (level of Ao arch prox per Reddy OpTechTCS)
  8. Belsey fundo (with EGD/bougie): 2 layers of interrupted sutures x2 progressively plicating fundus 240° around distal 2-3cm of esophagus (2nd layer includes crura/hiatus to secure fundo intra-abd)
  9. leak test
  10. close hiatus PRN (posterior crural stitches)
69
Q

typical esophageal stent sizes

A

typical/default: 23x100

available lengths: 60-150mm
available widths: 17-23mm

70
Q

EGD size

A

standard: 2.8mm channel = 9.8mm shaft = 29.4Fr
therapeutic/interventional: 3.7mm channel = 10.9mm shaft = 32.7Fr

71
Q

esophageal stent wire

A

super stiff 0.035” x 500cm (14cm tapered tip)
(Boston Scientific WALLSTENT Super Stiff Guidewire)

72
Q

endoscopic interventional wire sizing

A

diameter (in) x length (cm)

73
Q

thoracoabdominal incision

A

L posterolateral thoracotomy in 7th/8th rib space from ~2cm below tip of scapula to midpoint between xiphoid & umbilicus + circumferential diaphragm incision 1-2cm from attachment (mark matching points on both sides with clips to align it for closure) + excision costochondral cartilage segment

74
Q

safe distance from edge of central tendon for circumferential diaphragm incision

A

>5cm (mostly laterally, to avoid anterolat & posterolat branches)

75
Q

branches of phrenic nerve

A
  1. anterior & posterior trunks
  2. sternal + anterolat & crural & posterolat branches respectively
76
Q

positive DeMeester score for GERD

A

14.7

77
Q

muscle that must be divided for exposure of Zenker’s diverticulum/esophagus in surgical (cervical) rx

A

omohyoid (anterior belly)

78
Q

length of myotomy (of cricopharyngeus muscle) in Zenker’s diverticulum rx

A
  • proximal (cranial): 2cm into striated muscle (inferior pharyngeal constrictor/thyropharyngeus muscle)
  • distal (caudal): 2cm / fully divide cricopharyngeus up to 4cm (cricopharyngeus + 2cm of esophageal myotomy)
79
Q

bougie size for Zenker’s

A

36-40Fr (may place over wire ± endoscopic guidance)

80
Q

pyloroplasty v pyloromyotomy (technique & which is typically done for adults/post-esophagectomy)

A
  • pyloroplasty = Heineke-Mikulicz = pediatric (& Boffa post-esophagectomy) = full-thickness longitudinal division of pylorus & re-approximation transversely
  • pyloromyotomy = Ramstedt = adult/post-esophagectomy = partial-thickness division of muscle only (mucosa intact) ± coverage with omentum
81
Q

Which is more effective for emptying: pyloroplasty or pyloromyotomy?

A

pyloroplasty
(may actually have trouble with dumping)