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Module 16 > Esophageal & Gastric Disorders in the Horse > Flashcards

Esophageal & Gastric Disorders in the Horse Flashcards

1
Q

if the horse is not able to swallow what are the 3 categories of reasons why

A
  1. mechanical disorders
  2. anatomical abnormalities
  3. neurological
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2
Q

what are mechanical disorders that would prevent the horse from swallowing (5)

A
  1. persistent entrapment of epiglottis
  2. pharyngeal mass
  3. tongue foreign body
  4. tongue base neoplasia
  5. severe temporohyoid osteoathropathy
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3
Q

what are anatomical abnormalities that would prevent the horse from swallowing

A

palatoschisis

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4
Q

what would neurological reasons be for not be able to swallow (2)

A
  1. loss of pharyngeal sensation
  2. loss of normal coordination –> guttural pouch mycosis, guttural pouch neoplasia
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5
Q

what cranial nerve would cause pharyngeal paralysis

A

Glossopharyngeal

CN IX

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6
Q

What are the clinical signs of dysphagia (4)

A
  1. gagging and neck stretching when attempting to swallow
  2. nasal regurgitation of feed, saliva
  3. slow feed consumption
  4. particularly slow to eat forage
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7
Q

what could a diagnostic work up for dysphagia generally look like (8)

A
  1. oral exam: tongue base and ranula
  2. palpate retropharyngeal region (enlargement of lymph nodes?)
  3. palpate esophagus (left side, usually not palpable)
  4. can a stomach tube be passed?
  5. endoscopy of URT and guttural pouches
  6. endoscopic visualization of swallowing mechanism
  7. is pharyngeal sensation and response to stimulation normal
  8. radiographic investigation of pharynx
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8
Q

what are ddx to glossitis (3)

A
  1. tongue foreign body
  2. tongue squamous cell carcinoma
  3. sialolith
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9
Q

what is glossitis

A

inflammation/trauma of the tongue

due to foriegn body, tongue squamous cell carcinoma, sailolith

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10
Q

what would the diagnostic workup of glossitis entail (3)

A

may need to place probe

rad/CT to determine expense

histopathology to rule out neoplasia

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11
Q

how would you manage glossitis

A

debridement and lavage

topical, systemic metronidazole

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12
Q

what are the signs of temporohyoid osteoarthropathy be

A

slow chewing and deglutition

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13
Q

what nerve might be involved with temporohyoid osteoarthropathy

A

CN VIII

Vestibular nerve

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14
Q

what are the diagnostic features of temporohyoid osteoarthropathy

A
  1. endoscopic appearance
  2. decreased joint movement
  3. rad/CT to determine extent
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15
Q

how is temporohyoid osteoarthropathy managed

A
  1. conservative
  2. certahyoidectomy (disarticulating the affected side)
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16
Q

what is palatoschisis

A

cleft palate

embryonic palatal folds fuse rostral to caudal

can affect both hard and soft palate

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17
Q

what are the signs of palatoschisis

A

neonatal presentation or at weaning

difficulty nursing

aspiration pneumonia

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18
Q

where is the most common site for palatoschisis

A

cleft of caudal 1/2 to 2/3 of soft palate is most common

margins of cleft run caudally into palatopharyngeal arches

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19
Q

what would the symptoms of glossopharyngeal nerve (IX) damage be (3)

A
  1. chronic nasal discharge and slow ingestion
  2. possibly concurrent aspiration pneumonia
  3. intermittent epistaxis
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20
Q

how would you diagnose glossophrayngeal nerve damage

A

endoscopy of URT and guttural pouches to assess pharyngeal sensation and coordination

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21
Q

what are the reasons for glossopharyngeal nerve damage (2)

A
  1. guttural pouch mass (may need histopathology)
  2. guttural pouch mycosis
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22
Q

what is the diagnosis of this

A

granulomatous mass in guttural pouch

glossopharyngeal nerve damage

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23
Q

what is the prognosis of glossopharyngeal nerve damage due to mycosis

A

guarded

esophagotomy carries guarded prognosis due to risk of complications

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24
Q

what is equine dysautonomia

A

neurological disorder

grass sickness

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25
Q

what can equine dysautonomia cause (3)

A
  1. ptyalism
  2. dysphagia
  3. retrograde peristalsis

damage to enteric plexus plus cranial nerve nuclei

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26
Q

what is a linear esophageal ulceration

A

acute grass sickness

due to prolonged gastroesophageal reflux

may occur with gastric outflow obstruction

extreme pain on passage of NG tube

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27
Q

what is the clinical presentation of simple esophageal obstruction (4)

A
  1. most commonly soon after feeding
  2. bilateral nasal regurgitation of feed and saliva
  3. gagging/retching/neck stretching behaviour
  4. often coughing due to inhalation
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28
Q

how is esophageal obstruction diagnosis

A

feed material in green nasal discharge

resentment of cranial esophageal palpation

resistance to passage of NG tube

attempts to eat followed by coughing

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29
Q

how is a simple esophageal obstruction managed

A

heavy sedation and lavage via NG tube

sedation causes head to drop

gravity helps with drainage

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30
Q

what is the most common site of obstruction

A

dorsal esophagus, thoracic inlet and cardia

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31
Q

how would you lavage esophageal obstruction

A

under sedation

feed matieral exits via opposite nostril

if material is impacted at top of esophagus may be difficult to get horse to swallow

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32
Q

if its not possible to clear the esophageal obstruction completely what should you do

A

try again after few hours

remove feed and beeding and leave on water only

repeat procedure

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33
Q

what is the risk of simple esophageal obstructions

A

aspiration pneumonia at early stage

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34
Q

what else should you do to manage esophageal obstruction

A

NSAIDs to decrease pharyngeal pain

broad spectrum antibiotics necessary

maintain on soft diet for 7 days post relief of obstruction

consider thoracic rads to determine severity if choke of >12h duration

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35
Q

what are complications of choke

A

deep ulceration of esophagus

linear ulceration can precede rupture

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36
Q

how do you manage ulceration due to choke (3)

A
  1. sucralfate and omeprazole to minimize acidic gastroesophageal reflux
  2. dietary management
  3. complete hay replacement ration
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37
Q

what are secondary esophageal obstructions (4)

A
  1. pulsion diverticulum
  2. traction diverticulum
  3. stricture formation
  4. persistent right aortic arch
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38
Q

how would you manage a secondary esophageal obstruction

A
  1. depends on cause: pulsion vs traction
  2. surgery more likely to be required for full thickness mural cicatrix
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39
Q

what are the clinical signs of esophageal obstruction dilation (2)

A
  1. recurrent bouts of choke depending on size diverticulum
  2. tends to deteriorate with age in congenital cases due to poor wall tone
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40
Q

how could you diagnose recurrent esophageal obstruciton dilation (3)

A
  1. endoscopy
  2. double contrast esophagram
  3. radiograph to investigate aspiration
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41
Q

how would you manage recurrent esophageal obstruction dilation

A
  1. cervical pulsatile diverticuli can be repaired surgically
  2. can empty manually
  3. dietary management only for larger diverticuli
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42
Q

what are the clinical signs of esophgeal strictures (2)

A
  1. regurgitation of ingesta + saliva
  2. maybe history of neck trauma/bite
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43
Q

what is shown here

A

esophageal stricture

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44
Q

how are esophageal strictures managed

A

full thickness lesion requires esophagomyotomy to release mucosa

endoscopic assessment during surgery to determine success

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45
Q

how are esophageal strictures treated surgically

A

luminal diameter restored by longitudinal esophagomyotomy

separation of outer and inner layers of the esophageal wall

tube passed during surgery

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46
Q

what are the clinical signs of cervical esophageal rupture (4)

A
  1. swelling and pain at site of rupture
  2. may be draining tract
  3. subcutaneous emphysema
  4. cardiorespiratory compromise if mediastinitis
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47
Q

how would you diagnose cervical esophageal rupture (2)

A
  1. constrast esophagram
  2. may release feed material if debriding
48
Q

how are cervical esophageal rupture managed (5)

A
  1. immediate establishment of drainage to prevent mediastinitis
  2. surgical debridement is essential
  3. placement of tube orally or tube esophagostomy ventral to site (primary repair likely to dehisce)
  4. monitor for sepsis
  5. treatment of local cellulitis
49
Q

what clinical challenges with cervical esophageal rupture (6)

A
  1. maintenance of nutrient intake
  2. electrolyte balance
  3. concurrent aspiration pneumonia
  4. management of cellulitis
  5. possible endotoxemia, laminitis
  6. severe emphysema
50
Q

what are complications of cervical esophageal rupture (3)

A
  1. may succumb to complications of endotoxemia
  2. recurrent choke likely post recovery
  3. may be laryngeal hemiplegia due to sympathetic trunk damage
51
Q

what are clinical signs of thoracic/abdominal esophageal rupture (2)

A
  1. elevated temperature and resp rate
  2. progressive septic pleural effusion
52
Q

how would you diagnose thoracic/abdominal esophgeal rupture (3)

A
  1. esophageal endoscopy in unexplained pleural effusions
  2. thoracic ultrasound
  3. thoracocentesis & cytology
53
Q

how would manage thoracic/abdominal esophageal rupture

A

hopeless prognosis

rapid diagnosis most essential feature

liked to idiopathic muscular hypertrophy of esophagus in some cases

54
Q

where is the stomach located

A

left side

caudal to diaphragm and liver

55
Q

what side is the pylorus and duodenum

A

to the right

56
Q

what are the omental and ligament attachments of the stomach

A

to the liver, duodenum, pancreas, diaphragm and spleen

57
Q

how do you ultrasound the stomach

A

find the cranioventral border

follow dorsocaudally to determine size and filling

58
Q

what correltates with grastric volume when ultrasounding the stomach

A

height at ICS 12 correlates to gastric volume

59
Q

how thick should the stomach wall be

A

wall thickness ~9mm

60
Q

what is shown here

A

stomach

61
Q

where are the pyloric outflow and duodenum landmark when US the stomach

A

right ICS 10-11

duodenum cranial to pole of right kidney

ultrasound window between right liver and right dorsal colon

62
Q

what is the wall thickness of the duodenum

A

<4mm

63
Q

what are clinical signs with acute gastric distention (4)

A
  1. acute colic
  2. possible rupture
  3. peritonitis
  4. endotoxemia
64
Q

what are the clinical signs with chronic gastric distention (4)

A
  1. weight loss and reduced rate of feed intake
  2. increased water intake
  3. recurrent mild colic
  4. pendulous abdomen +/- ventral edema
65
Q

what are clincal signs of chronic gastric inflammation (2)

A
  1. may be symptom free, progressing to acute colic
  2. change in dietary preference
66
Q

what are the clinical signs of chronic gastric ulceration (2)

A
  1. loss of performance; decreased forward movement
  2. anterior abdominal pain
67
Q

what are parasitic infections of the gastric

A

gasterophilus larvae

68
Q

what are dysmotility gastric disorders (4)

A
  1. equine dysautonomia
  2. acute gastric dilation
  3. gastric impaction
  4. chronic gastric dilation
69
Q

what are ulcerative gastric disorders

A

equine gastric ulceration syndrome

perforation and rupture

70
Q

what are gastric neoplastic disorders

A

squamous cell carcinoma

71
Q

what are inflammatory equine gastric disorders (2)

A
  1. inflammatory polyps
  2. glandular ulceration and gastritis
72
Q

what are risk factors for acute gastric dialtion (2)

A
  1. excess or fermentable feed
  2. incorrect management
73
Q

what are clinical signs of acute gastric dilation (4)

A
  1. acute abdominal pain
  2. spotaneous nasogastric reflux
  3. progressive acidosis
  4. endotoxemia
74
Q

how is acute gastric dilation diagnosed

A

based on presentation

75
Q

how is acute gastric dilation treated (4)

A
  1. gastric decompression and lavage
  2. IV fluid support
  3. correction of acidosis
  4. management of endotoxemia
76
Q

what are sequelae to endotoxemia in acute gastric dilation (2)

A
  1. laminitis
  2. acute renal failure
77
Q

what are gastric complications that can occur during acute gastric dilation (3)

A
  1. transient loss of motility
  2. delayed emptying
  3. serosal tear
78
Q

how do you manage the complications of acute gastric dilation (4)

A
  1. gastroscopic assessment
  2. risk fo secondary impaction
  3. complete pelleted ration
  4. altered feeding freq
79
Q

what are risk factors for acute gastric impactions (5)

A
  1. poor dentition
  2. old age
  3. trichobezoars (hair ball)
  4. persimmon seeds
  5. inappropriate feeding
80
Q

what are the clinical signs of acute gastric impactions (3)

A
  1. acute colic presentation
  2. endotoxemia
  3. possible rupture
81
Q

how are acute gastric impactions diagnosed (3)

A
  1. resistance to stomach tube
  2. ultrasonography
  3. gastroscopy
82
Q

how are gastric impactions managed (2)

A
  1. gastric lavage: remove soluble material
  2. continuous lavage
83
Q

how would you do continuous lavage to treat gastric impactions

A

5L/hour as continuous infusion via indwelling tube

position in terminal esophagus

alterante electrolytes with water to prevent Na+ overload

daily mineral oil

84
Q

how long might it take for a gastric impaction to resolve

A

may take 3-6 days

85
Q

what are the risk factors of chronic gastric impactions

A

not known

increased in warmbloods

86
Q

what are the clinical signs of chronic gastric impaction (5)

A
  1. failure to gain weight/weight loss
  2. change in abdominal silhouette
  3. change in demeanour
  4. ventral edema
  5. acute colic +/- prior recurrent colic
87
Q

how are chronic gastric impactions diagnosed (5)

A
  1. resistance to stomach tube
  2. enlarged gastric outline
  3. stomach may be palpable
  4. gastroscopy: impaction often vertically stacked
  5. may be up to esophageal cardia
88
Q

how do you treat chronic gastric impactions

A

prolonged continuous gastric lavage

aim to empty stomach

89
Q

how do you manage chronic gastric impactions (3)

A
  1. permanent turnout
  2. no forage other than grass
  3. complete pelleted ration if required
90
Q

what is the prognosis of chronic gastric impactions

A

progressive further dilation of stomach, spontaneous rupture possible

2-4 years from presentation

dependent on speed of initial diagnosis

lifelong diligent management

91
Q

what are the risk factors of equine gastric ulceration syndrome (EGUS) (8)

A
  1. decreased access to grazing
  2. high intake of concentrate rations
  3. prolonged periods without forage
  4. intesive training at >70% VO2max
  5. other GI disorders
  6. NSAIDs
  7. crib biting
  8. pregnancy
92
Q

what are the clinical signs of equine gastric ulceration syndrome (EGUS) (3)

A
  1. loss of performance
  2. decreased feed intake
  3. colic as severity increases
93
Q

how is equine gastric ulceration syndrome (EGUS) diagnosed (2)

A
  1. gastroscopy
  2. sucrose absorption may be herd screening tool
94
Q

what are stratified squamous ulceration scores

A

scored from 0-1 with lesions > 3 of clinical significance

95
Q

what is stratified squamous ulceration based on

A

surface area is primary determinant of score

96
Q

grade these ulcerations

A

grade 0

grade 1

grade 2

97
Q

what grade is this ulcer

A

grade 3

98
Q

what grade is this ulcer

A

grade 4

99
Q

what is grandular ulceration

A

mostly scored from 0-4

gross appearance of lesions very variable

erythema to ulceration

100
Q

what grade is this glandular ulcer

A

grade 0

101
Q

what grade is this glandular ulcer

A

grade 1

102
Q

what grade is this glandular ulcer

A

grade 2

103
Q

what grade is this glandular ulcer

A

grade 3

104
Q

what grade is this glandular ulcer

A

grade 4

105
Q

what lesions are more siginficant in glandular ulceration (think location)

A

lesions affecting pyloric motility

106
Q

what are the gross appearance of glandular inflammatory lesions (6)

A
  1. erythema
  2. flat, hemorrhagic
  3. raised, hemorrhagic
  4. flat, diptheritic
  5. raised diptheritic
  6. combination
107
Q

what are the presenting signs of equine glandular polyps (3)

A
  1. recurrent colic
  2. weight loss
  3. short episodes of acute pain
108
Q

what is prognosis of equine glandular polyps based on

A
  1. size
  2. response to treatment
109
Q

how are squamous erosion and ulceration treated with EGUS

A

omeprazole 4mg/kg SID 4-6 weeks

tapered dose for 2 weeks

sucralfate 20mg/kg 3-4 x daily

110
Q

how can squamous erosion and ucleration in EGUS be managed (5)

A
  1. increased access to forage and grazing
  2. decreasd or stop concentrate feed
  3. decreased intesity of exercise
  4. chaff feeds prior to exercise
  5. reduce other stressors
111
Q

how are squamous erosion and ulceration in EGUS prevented

A

improved management to reduce risk factors

gastroguard 1mg/kg at start of training

112
Q

how are glandular ulceration and inflammation in EGUS treated

A

longer term depending on type of lesion

omeprazole 4mg/kg SID 4-6 weeks + reassessment prior to reducing

sucralfate 20mg/kg x3 daily

113
Q

how are refractory glandular ulcerative lesions of EGUS treated

A

diphtheritic membrane or inflammation

addition of doxycycline 10mg/kg BID in sucralfate carrier (muco-adhesive)

further 4wk course of omeprazole

114
Q

what additional therapies can be used to treat glandular ulcertive EGUS lesions

A
  1. pectin-lecithin complex may be beneficial
  2. antacids? multiple unproven supplements
115
Q

how are inflammatory polyps treated in EGUS

A

similar treatment initially

longer treatment course

lifelong management to prevent obstruction of pyloric canal

strict dietary control

116
Q

what further investigations are needed if you diagnose inflammatory polyps in EGUS

A

histopathological investigation

freq and significance of lesions

assessment of risks

rational approach to management and prevention

Module 16 (26 decks)

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