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TnJ > 90. Esophagus > Flashcards

90. Esophagus Flashcards

1
Q

nerve supply that travels with thoracic esophagus into abdomen

A

dorsal and ventral vagal trunkscranially: pharyngoesophageal n, recurrent laryngeal nerves, paralaryngeal n, vagal n.

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2
Q

T/Fthe esophagus has a serosal outer layer

A

FALSEadventitia

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3
Q

diffierence in muscular composition of the esophagus in dogs vs cats

A

dogs—entirely skeletal musclecats—skeletal muscle and terminates as smooth muscle, terminal portion folds transversely (herringbone)

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4
Q

sphincters of the esophagus

A

had to ddx anatomicallycranial: cranial esophageal sphincter (made of cricopharyngeal/thyropharyngeal muscles)caudal: lower esophageal sphincter (gastroesophageal junction–hi P)

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5
Q

main blood supply to the esophagus

A
  1. cervical esophagus: cranial and caudal thyroid arteries2. thoracic esophagus cranial 2/3: bronchoesophageal artery3. thoracic esophagus caudal 1/3: esophageal branches of aorta and dorsal intercostal arteries4. terminal abdominal esophagus: left gastric artery
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6
Q

3 phases of swallowing

A
  1. oropharyngeal (oral (voluntary), pharyngeal (involuntary), pharyngoesophageal/cricopharyngeal): prehend, masticate, make bolus, push through cricopharyngeal sphincter (protect nasopharynx with contraction of palatal/pharyngeal constriction to close, caudal epiglottis reflection and vocal fold adduction to protect airway); final stage is relaxation of muscles while delivering bolus to cranial esophagus2. esophageal: primary peristaltic wave stimulated by dissension from bolus, pushes aborally; second wave will occur if dissension remains in esophagus3. gastroesophageal: muscularis relaxes ahead of the bolus and the bolus is propelled through gastroesophageal sphincter
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7
Q

nerves responsible for oropharyngeal stage of swallowing

A

5 trigeminal 7 facial9 glossopharyngeal10 vagus12 hypoglossal

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8
Q

in healthy dogs, esophageal transmit time with liquid vs kibble

A

DEPENDS ON POSITIONING!sternal: 3 (liquid) -4 (kibble) minR lateral recumbency: 7(liquid) –9 (kibble) minfaster in STERNAL

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9
Q

general causes of dysfunction of the esophagus

A
  1. mechanical (or anatomic) lesions: FB, tumors, strictures, vascular ring anomalies, intussusceptions, hiatal hernias2. functional (or NM) lesions: hypoperistalsis/aperistalsis3. inflammatory lesions: acute vs chronic
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10
Q

reasons why esophagus has higher prevalence of incisional dehiscence

A
  1. lack serosa (heals create fibrin seal and source of stem cells)2. segmental blood supply3. lack omentum4. constant motion5. tension at surgical site
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11
Q

T/Fcan ligate branches supplying thoracic esophagus and it will live

A

TRUE as long as cervical and abdominal portions are intact due to strong intramural blood plexuses in the submucosaCANNOT ligate cervical and thoracic segments at the same time (necrosis)

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12
Q

surgical approaches to the esophagus

A
  1. ventral midline2. cranial median sternotomy3. right and left lateral thoracotomies depending on lesion
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13
Q

suture holding layer of esophagus

A

submucosa

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14
Q

resection of how much of the esophagus has been associated with an increased rate of dehiscence

A

resection of > 3-5 cm of esophagus has been associated with increased dehiscence

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15
Q

considerations for a two layer closure in the esophagus

A
  1. intraluminal knots simple interrupted of submucosa, mucosa2. extraluminal knots inverting pattern or appositional simple interrupted(can consider simple interrupted or continuous single layer but interrupted is preferred)
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16
Q

what is the maximum cervical and thoracic esophagus that can be resected in experimental dogs

A

20% cervical 50% thoracicCAUTION: TENSION

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17
Q

method to relieve tension on esophageal R&A

A

circumferential PARTIAL myotomy of outer muscle layer (to heal by 2nd intention) caution with excessive mobilization due to disruption of the segmental blood supply

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18
Q

methods of esophageal R&A

A

–simple interrupted closure–end to end stapling devices–biodegradable anastomic ring–esophageal substitution

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19
Q

esophageal patching

A

omentum, pericardium, SIS, muscle (sternothyroid, longus colli), buccal mucosal graftscan be used to reinforce closure (on-lay)can be used following esophagoplasty after longitudinal division of esophageal stricture (in-lay)

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20
Q

esophageal substitution

A

if massive resectioncan replace cervical esophagus with inverse tubed skin graft; can also use muscle grafts, gastric advancement for other areas of esophagus to be replacedmultistage procedureMINIMAL clinical experience

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21
Q

in embryos, what are the great vessels derived from

A

paired dorsal and ventral aortas and the 6 interconnecting pairs of aortic arches (6 brachial arches)arches 1,2 involute3rd arches becomes carotid arteriesleft 4th AA –> adult aortic archright 4th–> right subclavianleft 6th AA–>pulmonary trunk, ductus arteriosus (ligamentum arteriosus)right 6th–>pulmonary artery

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22
Q

7 types of vascular ring anomalies

A
  1. PRAA with left LA (most common 95%)2. PRAA with right LA (NO ring, no obstruction)3. PRAA with aberrant LEFT subclavian artery and right LA (artery passes dorsal from the right sided Ao–single ring incomplete stricture)4. PRAA with aberrant left subclavian and Left LA (double ring strictures)5. Double AA (significant tracheal stenosis)6. normal AA (left) with persistent right LA (mirror image of PRAA and left LA–NEEDS A RIGHT LATERAL THORACOTOMY)7. aberrant right subclavian (arising from Ao instead of brachiocephalic trunk and travels dorsal across esophagus–partial ring, may not see clinical signs, but is common)
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23
Q

in PRAA patients with LA, how often is the ligamentum patent (ductus)? And what other abnormality may be present

A

left cranial vena cava 45%patent ductus 10%other congenital abnormalities 20%

24
Q

signalment for PRAA

A

GSD, Irish Setter> 15 kg20% diagnosed by 2 months80% diagnosed by 6 months

25
Q

diagnostic imaging for diagnosis of PRAA

A

–survey films (cranial focal dilation, check aspiration, VD right Ao and left deviation trachea)–positive contrast radiography (barium)–fluoroscopy–angiography–echocardiography–CT/MRI–Esophagoscopy (rule out other causes of esophageal obstruction, look what side aortic pulse is)

26
Q

only vascular ring anomaly that cannot be addressed through a left lateral thoracotomy

A

normal AA (left) with a RIGHT LAnormal PRAA with left LA approach: left 4th in dogs, left 5th in cats

27
Q

what structure wraps around the ligamentum arteriosus

A

left recurrent laryngeal nerve

28
Q

why can you ligate and divide the subclavian arteries

A

collateral flow through vertebral artery

29
Q

diagnosis and approach to double AA

A

both aortic arches contributeangiography would tell which side is contributing moreapproach, ligate, divide and oversew smaller side

30
Q

prognosis and post op complications

A

continued regurgitation (NM functional loss, muscle atony)aspiration pneumoniadeath

31
Q

prognosis of PRAA surgery in 1980s Shires and Liu

A

3 week survival 80%intermittent regurgitation present in 67% (2/3)poor outcome in 25%

32
Q

Muldoon et al 2003 prognosis of PRAA

A

2 week survival 95%92% had complete resolution of all clinical signs8% had a “good” outcome50% dogs had follow up radiographs and all had radiographic evidence of megaesophagus

33
Q

prognosis and reported surgery for congenital megaesophagus

A

hi mortality 75% die within a yresophagodiaphragmatic cardioplasty using the Torres technique (cut L diaphragm, trim, and resuture)–small case series

34
Q

most common esophageal FB in dogs vs cats

A

dogs: ingested bones**cats: fish hooks, needles, string

35
Q

common locations for esophageal FB

A

thoracic inletheart base (10-30%)caudal esophagus (70-80%)

36
Q

success of FB retrieval with endoscopy

A

60% retrieved30% pushed into stomach10% required surgery

37
Q

T/Facute esophageal penetrating injuries have a poorer prognosis that oropharyngeal injuries

A

TRUE36% mortality

38
Q

acquired vs congenital esophageal strictures

A

congenital (rare)acquired–damage extending to muscular layer, heals by fibrosis and wound contracturemost common injury causing stricture—REFLUX 50% in dogs

39
Q

esophageal strictures in cats has been associated with what oral drug (s)

A

doxycyclineclindamycinretention of tablets causes focal esophagitis and subsequent stricture formationgive with water

40
Q

diagnosis of esophageal stricture

A

–positive contrast esophagogram –esophagoscopy (allows biopsy and treatment in same episode)–fluoroscopy60-75% single (caudal thoracic esophagus) 40% multiple

41
Q

treatment for acquired esophageal strictures

A

–bougienage (longitudinal shear force)–balloon dilatation (radial force to open)+/- esophageal stents+/- depository GCC, mitomycin cmay need multiple attempts for dilation–surgery reserved for failed therapy (esophagoplasty–patch or simple, R&A, esophageal substitution–free skin tube flap, free jejunal segment)

42
Q

outcome following dilatation with bougienage or balloon dilatation for esophageal strictures

A

70-90%may need multiple episodes

43
Q

traction vs pulsion diverticulum of the esophagus

A

pulsion –mucosa out pouch through defect in tunica muscularistraction–full thickness deviation of the esophageal wall

44
Q

where is an epiphrenic diverticula located

A

btwn heart base and diaphragm

45
Q

in relation to time after anesthesia, when do acquired esophageal strictures occur

A

~3 weeks after anesthesia

46
Q

T/Fbronchoesophageal fistula are more common in dogs than tracheoesophageal fistula

A

TRUEbronchoesophageal fistula most frequently communicate with right caudal lung lobe bronchusexcise and repair rather than just ligatepx depends on how extensive the lung pathology is

47
Q

cricopharyngeal dysphagia

A

swallowing disorder–congenital, dx < 12 mocharacterized by cricopharyngeal achalasia (failure of upper esophageal sphincter to open/relax) or asynchrony (incoordination)food remains in pharynxfailure of the cricopharyngeal phase of swallowing

48
Q

diagnosis of cricopharyngeal dysphagia

A

oral examendoscopic examsurgery films (generally normal)definitive dx fluoroscopy with visualization of swallow–normal bolus formed, normal pharyngeal contraction, but failure of RELAXATION of cricopharyngeal muscles/sphincter

49
Q

differential to cricopharyngeal dysphagia

A

–pharyngeal dysphagia (weak contraction)important to ddx bc cricopharyngeal myotomy improves cricopharyngeal dysphagia but worsens pharyngeal dysphagia

50
Q

treatment for cricopharyngeal dysphagia

A

cricopharyngeal myotomy or myectomy +/- thyropharyngeal myotomy (use hemoclips to ID post op)placement of orogastric tubecricopharyngeal muscle (single unpaired)O: lateral side of one cricoid spreads dorsally over esophagusI: contralateral cricoid cartilageinnervated by glossopharyngeal (9), vagus–pharyngeal branch (10)blood supply: cranial thyroid artery

51
Q

how is the cricopharyngeal muscle approached for treatment of cricopharyngeal dysphagia

A

ventral midline (have to rotate larynx 180 degrees with stay sutures)orlateral (preferred)remove 2-2.5 cm of cricopharyngeal muscle

52
Q

prognosis of cricopharyngeal dysphagia

A

treated young—px good to excellentimmediate alleviation of clinical signs 13/14 dogscomplete resolution only 50%recurrence possible with fibrosis/contracture of surgery siteno diff myotomy vs myectomy or surgeon experiencepoorer outcome if concurrent esophageal dysfx or stricture, underlying NM disease etc

53
Q

esophageal neoplasia

A

SCC (#1 in cats)leiomyosarcoma/leiomyoma (B)OSAFSA (sarcoma related—spirocerca lupi)plasmacytoma (B)usually advanced, met 50%generally poor prognosis unless benign

54
Q

most common location of esophageal neoplasia in dogs vs cats

A

dogs–caudal thoracic esophaguscats–cranial thoracic esophagus

55
Q

percentage of dogs with spirocerca lupi related esophageal sarcoma and hyper tropic osteopathy

A

40%

TnJ (128 decks)

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