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SA Alimentary > Regurgitation and vomiting > Flashcards

Regurgitation and vomiting Flashcards

1
Q

What clinical features in the dog or cat make you think it has oropharyngeal dysphagia?

A

Hunger with multiple messy attempts to eat

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2
Q

Pharyngeal retching

A

Food and saliva brought back immediately.

Difficulty +/- pain and distress on attempted swallowing.

Repeated unsuccessful attempts at swallowing. Liquids may come back down nose if severe (nasal discharge)

May be anorexic and cachexic.

Aspiration (with resultant pneumonia and cough) common.

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3
Q

Regurgitation

A

More passive than vomiting - lowers head with no abdominal effort.

Tube of undigested food + white saliva (usually not bile-stained) falls out.

Can be soon after feeding or delayed several hours - ingesta sits in dilated oesophagus and regurgitation triggered by increased intrathoracic pressure

Often bright and try to eat it again.

Aspiration pneumonia and cachexia common.

Uncommon in cats

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4
Q

True vomiting

A

Active process involving reflex and muscular contractions.

Usually preceded by nausea (prodromal signs e.g. agitation, salivation, swallowing, lip smacking).

Forceful ejection of vomit.

Less likely to eat vomitus afterwards (but may do).

Vomit may be partially digested food, fluid (often bile stained) and/or haematemesis.

Aspiration pneumonia unusual

pH is a poor indicator but would expect stomach contents to have low pH

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5
Q

Congenital abnormalities that could cause vomtining/regurgitation

A

Vascular ring anomaly

Oesophageal diverticulum

Broncho-oesophageal fistula

Hiatal hernia

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6
Q

Most common dog breed to get foreign body in the oesophagus

A

West highland white terrier

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7
Q

Which breeds are overrepresented for regurgitation and hiatal hernia?

A

Brachycephalic dogs

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8
Q

What disorder could be worse when ingesting liquid?

A

pharyngeal dysphagia

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9
Q

Which disorders could be worse when ingesting food (rather than liquid)?

A

crichophalangeal achalasia
oesophagitis

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10
Q

What could cause gas in the oesophagus on radiograph?

A

Megaoesophagus

Vascular ring anomaly

Stricture

Severe oesophagitis

Aerophagia

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11
Q

What can cause aerophagia?

A

Excitement

Nausea

Anaesthesia/GA

Dyspnoea

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12
Q

Innervation of the pharynx

A

IX and X sensory and motor

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13
Q

Anatomy of oesophagus

A

mucosa, submucosa with mucous glands, muscularis + loose connective tissue (no serosa)

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14
Q

Canine muscularis muscle of the oesophagus

A

Two intertwining layers of striated muscle

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15
Q

Feline muscularis muscle of the oesophagus

A

Cranial and middle sections mixed smooth and striated

terminal 35% entirely smooth muscle

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16
Q

Upper oesophageal sphincter

A

cricopharyngeal sphincter (cricopharyngeal and thyropharyngeal muscles).

Relaxation co-ordinated with swallowing.

Prevents aerophagia and reflux of food from oesophagus into pharynx

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17
Q

Lower oesophageal sphincter

A

gastro-oesphageal sphincter = not a true sphincter but “distal high pressure zone” (inner layer of gastric smooth muscle with outer oesophageal striated muscle in dog + contributions from diaphragm and intra-abdominal pressure).

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18
Q

Swallowing

A

Ingesta pushed to caudal part of mouth by movement of base of tongue against hard palate

Hyoid apparatus moves larynx cranially, base of tongue moves caudally, epiglottis flips up over larynx and bolus forced through relaxed UOS to proximal oesophagus

Larynx then moves caudally again and epiglottis returns to original position under soft palate

Oesophagus stimulated by stretch -> primary peristaltic wave which propels food to stomach

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19
Q

Differential diagnoses of pharyngeal retching/dysphagia

A

Oropharyngeal trauma

Oropharyngeal foreign body

Oropharyngeal inflammation

Oropharyngeal mass

Salivary mucocoele, polyp, abscess

Neurological and muscular problems

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20
Q

Oropharyngeal trauma

A

Mandible

Maxilla

TMJ

Hyoid bones

Soft tissue

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21
Q

Oropharyngeal inflammation

A

Gingivitis

Stomatitis

Pharyngitis

Tonsillitis

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22
Q

Oropharyngeal masses

A

Tonsillar squamous cell carcinoma

Peripharyngeal lymphoma

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23
Q

Neurological and muscular problems leading to pharyngeal retching or dysphagia

A

Masticatory myositis

Cranial nerve deficits e.g. V (trigeminal neuritis - often just motor), VII, IX, X.

Pharyngeal dysphagia

Dysautonomia

Botulism

Rabies

Myasthenia gravis (focal form: extraocular muscles, V, VII, IX ± oesophagus)

Cricopharyngeal achalasia or stenosis

Idiopathic hypersialosis

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24
Q

Cricopharyngeal achalasia

A

Upper oesophageal sphincter = cricopharyngeal sphincter (cricopharyngeal and thyropharyngeal muscles)

Rare congenital (v. rarely acquired). Cocker spaniels

Disrupted co-ordination between cricopharyngeal relaxation and swallowing

Cricopharyngeus remains contracted during swallowing.

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25
Q

Clinical signs of cricopharyngeal achalasia

A

Severe dysphagia

Distress

Rhinitis

Aspiration

Weight loss

Often anorexia

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26
Q

Diagnosis of cricopharyngeal achalasia

A

History

Fluoroscopy during barium swallow

+/- manometry muscle

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27
Q

Treatment of cricopharyngeal achalasia

A

No successful medical treatment

Cricopharyngeal myotomy often curative

Important to differntiate from pharyngeal dysphagia as myotomy makes pharyngeal dysphagia worse

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28
Q

Pharyngeal dysplasia

A

Almost invariably acquired.

Often old.

Often idiopathic due to reduced pharyngeal sensation or due to variety of neuropathies (cranial nerves IX and X) and perhaps myopathies (e.g. local myasthenia gravis).

May have concurrent laryngeal paralysis (do not tie back!).

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29
Q

Clinical signs of pharyngeal dysphagia

A

Like cricopharyngeal achalasia but often more dysphagia with fluids than solids - less likely to sense presence of fluids in pharynx.

Aspiration of fluids common - proximal oesophagus often concurrently flaccid (also innervated by IX and X) leading to pooling of food which is later regurgitated and aspirated.

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30
Q

Treatment of pharyngeal dysphagia

A

No treatment for idiophathic

Cricopharyngeal myopathy makes it worse

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31
Q

Idiopathic hypersialosis

A

recently reported condition in dogs (± cats?) with painful salivary gland enlargement, gagging, retching and hypersalivation.

Salivary gland biopsies are normal.

Dogs respond rapidly to phenobarbitone therapy, prompting the suggestion this may be an unusual limbic form of epilepsy, but can often wean off therapy long term (unlike epilepsy).

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32
Q

Anatomical differential diagnoses of regurgitation

A

Vascular ring anomaly

Hiatal hernia

Oesophageal diverticulum

Broncho-oesophageal fistula

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33
Q

Differential diagnoses for oesophagitis causing regurgitation

A

Trauma

Reflux (GA, Hiatal hernia, poor sphincter function)

Irritant (drugs, dietary indiscretion)

Secondary to megaoesophagus

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34
Q

Neuromuscular causes of regurgitation

A

Idiopathic megaoesophagus

myasthenia gravis,

myositis,

myopathy,

neuritis,

peripheral neuropathy,

central (brainstem disorders),

hypothyroidism,

hypoadrenocorticism,

toxicity (lead, thallium, anticholinesterase),

dysautonomia,

Sialoadenosis

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35
Q

Obstructive causes of regurgitation

A

Oesophageal foreign body (FB)

Oesophageal stricture

Gastroesophageal intussusception

Oesophageal and peri-oesophageal masses

Oesphageal mural neoplasia

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36
Q

Oesophageal foreign body signalment

A

Most common in terriers, particularly Westies

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37
Q

Oesophageal foreign body

A

Usually lodge in the thoracic inlet OR over heart base OR distal oesophagus

Often bone- if partial obstruction may keep fluids down but not solids

Emergency - high risk of pressure necrosis of oesophagus

Possible sequelae: chronic stricture formation, erosion causing mediastinitis, and/or vascular erosion

Chronic cases show dilation of oesophagus proximally +/- broncho-oesophageal fistulae

Possible aspiration pneumonia

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38
Q

Diagnosis of oesophageal foreign body

A

Radiography - always do plain films first

FB +/- mediastinitis +/- aspiration pneumonia +/- air in dilated oesophagus proximal to FB

Contrast may be used outline radiolucent FBs + delineate perforated areas or fistulae

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39
Q

Treatment of oesophageal foreign body

A

Preferably remove endoscopically or push on to stomach.

Replace fluid/electrolyte deficits prior to GA. Note in some foreign body moves on unaided as pre-med/GA relaxes muscles.

Thoracotomy if unsuccessful - poorer prognosis.

Treat mediastinitis, pneumonia and oesophagitis aggressively.

Do not use naso-oesophageal feeding tubes post removal.

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40
Q

Oesophageal strictures secondary to oesophagitis

A

46-655 due to reflux during GA

Treatment:
- Balloon dilation
- Bougienage
- +/- Transendoscopic triamicolone injection
- post operatively food should have a firm consistency to continually dilate the stricture after discharge
- repeat procedures common
- complication: oesophageal perforation

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41
Q

Megaoesophagus

A

common cause of regurgitation in dogs.

Also cats (less common).

Congenital and acquired forms.

Oesophagus becomes dilated and hypomotile (but note gastro-oesophageal sphincter still relaxes normally - not equivalent to achalasia in man where gastro-oesophageal sphincter fails to dilate - in dogs, primarily oesophageal dysfunction)

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42
Q

Congenital megaoesophagus

A

Increased incidence in Irish setters, great Danes, GSDs, Labrador retrievers, Chinese shar-peis and Newfoundlands and suspected inherited, but inheritance only shown in miniature schnauzers (dominant 60% penetrance) and wirehaired fox terriers (recessive).

Also found in Siamese cats with concurrent pyloric stenosis.

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43
Q

Acquired megaoesophagus

A

most commonly idiopathic.

Also secondary particularly to neuropathies/myopathies and metabolic disease:
* 25% of dogs have myasthenia gravis: congenital or acquired; generalised or localised to the oesophagus and head
* Feline dysautonomia
* Labrador retriever myopathy
* Myositis
* Toxicity: botulism; lead poisoning
* Brainstem disease including distemper virus and some brain tumours
* Some peripheral polyneuropathies e.g giant axonal neuropathy in GSDs, acquired sensory neuropathies
* Addison’s disease.
* Prolonged partial or complete obstruction

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44
Q

Diagnosis of megaoesophagus

A

Usually chronic history of passive regurgitation.

Often concurrent cough ± pyrexia due to aspiration pneumonia.

May be concurrent oesophagitis - more discomfort and more severe signs

Plain radiographs often show dilated oesophagus with air± ingesta.
Dorsal tracheal stripe sign ± tracheal depression.
Aspiration pneumonia - classically dependent areas middle and caudal lung lobes.

Contrast radiographs: barium with meat or paste (liquid may not delineate dilation well) ± fluoroscopy. Care to avoid aspiration. Do not need contrast in all cases – only if not visible on plains.

Oesophagoscopy best avoided unless suspect underlying cause e.g. foreign body or tumour - GA and scoping increases risk of aspiration, gastro-oesophageal reflux and oesophagitis.

If acquired, check for underlying causes including blood screens (+ electrolytes), serology for acetylcholine receptor antibodies (± repetitive nerve stimulation of peripheral muscles - abnormal in myasthenia gravis even if clinical signs restricted to oesophagus).

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45
Q

Treatment of megaoesophagus

A

no specific treatment restores oesophageal function.

Treat underlying cause early).

Reduce risk of aspiration and assist oesophageal function:

  • Feed little and often from a height + water from a height. Raise frontlegs after feeding.
  • Avoid exercise after feeding.
  • Type of food: some best with soft food and some with dry food so adjust to individual.
  • Often cachexic - feed high energy diet - lots of fat and protein.
  • Consider gastrostomy tube if seriously malnourished. Naso-oesophageal tubes clearly contra-indicated.
  • Aggressive antibiosis if aspiration pneumonia - iv to ensure absorbed initially.
  • Very important to manage any concurrent oesophagitis with drugs

GI PROMOTILITY DRUGS CONTRAINDICATED

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46
Q

Gastro-oesophageal reflux/oesophageal hypomotility

A

It is possible to have GO reflux and oesophageal hypomotility without overt mega-oesophagus.

particularly in terriers and esp Border terriers

It resolves in many cases with time (by > 1 year of age) but can be clinically apparent

Affected dogs tend to regurgitate and bring up some bile

Diagnosis usually requires a swallowing study (fluoroscopy)

Treatment involves a low fat diet, sucralfate paste and acid inhibitors

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47
Q

Vascular ring anomaly incidence

A

Relatively common in dogs - also cats.

Higher incidence large breeds e.g. GSDs and Irish Setters (which can also have idiopathic megaoesophagus).

Suspected familial.

No specific cat breeds.

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48
Q

Possible vascular ring anomalies

A

Number of possible VRAs - due to defects in normal development of arteries from the 6 pairs of fetal aortic arches.

Only clinical problem if anomaly causes constriction of oesophagus over base of heart.

95% of reported cases = persistent right aortic arch (PRAA) -> oesophageal constriction

Other significant anomalies are: aberrant right or left subclavians; persistent double aortic arch (tend to result also in tracheal obstruction); aberrant intercostals and persistent right ligamentum arteriosum with normal left aortic arch.

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49
Q

VRA and megaoesophagus

A

cause chronic partial obstruction over heart base with acquired megaoesophagus cranial to it and, chronically, megaoesophagus may develop caudally as well.

Some degree of megaoesophagus always present at diagnosis.

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50
Q

Diagnosis of vasucalr ring anomalies

A

Often present at weaning but may be older

Cope with liquid/gruel better than food

May have concurrent oesophagitis and aspiration pneumonia

Plain lateral thorax films

Contrast studies

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51
Q

Vascular ring anomalies on plain radiographs

A

Dilated cranial thoracic oesophagus and ventral deviation of the trachea

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52
Q

Contrast studies with vascular ring anomalies

A

May not be necessary

Use barium and meat not just fluid

Constriction over heart base

+/- fluoroscopy to assess motility of caudal oesophagus

Significant risk of aspirating the contrast material- can cause an inflammatory reaction

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53
Q

Treatment of vascular ring anomalies

A

Manage the megaoesophagus ± oesophagitis ± aspiration pnemonia ± cachexia

Then surgery e.g. ligate ligamentum arteriosum if persistent right aortic arch.

Warn owner of likely permanent oesophageal hypomotility - regurgitation may continue after surgery.

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54
Q

Gastro-oesophageal reflux

A

occurs when there is temporary or permanent gastroesophageal sphincter (GOS) incompetence

Results in oesophagitis

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55
Q

Causes of gastro-oesophageal reflux

A

chronic vomiting;

post GA;

hiatal hernias;

gastric motility disorders;

masses in the region of the GOS.

May occur overnight during sleep -> early morning salivation and regurgitation (ddx from more common early morning bilious vomiting syndrome).

Also suspect high incidence in young terriers.

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56
Q

Gastro-oesophageal reflux under GA

A

significant reflux occurs small number of patients in spite of good anaesthetic technique.

GA predisposes to reflux - anaesthetic and sedative drugs tend to reduce GOS pressure, reduce oesophageal peristalsis to remove refluxed material and reduce production of saliva which would normally neutralise refluxed acid in oesophagus.

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57
Q

Oesophagitis

A

Usually secondary to chronic gastritis and vomiting, gastroesophageal reflux, ingestion of foreign body or caustic material, hiatal hernia, neoplasia or megaoesophagus.

Inflammation of mucosa ± submucosa and muscularis.

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58
Q

Oesophageal stricture

A

Fibrosis and narrowing of oesophagus in one or more places.

Can be congenital but usually acquired

Occurs up to 14 days after gastroesophageal reflux post GA - may show few signs prior to stricture formation.

May have one or several strictures - often several if due to GA reflux: in thoracic inlet, over base of heart and/or distal high pressure zone.

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59
Q

Diagnosis of Gastroesophageal reflux, oesophagitis and oesophageal stricture

A

History and clinical signs

Plain ± contrast radiographs essential to show any underlying cause ± aspiration pneumonia

If stricture formation: plain films show megaoesophagus cranial to stricture in some ± aspiration pneumonia ± underlying cause or plain radiographs may be normal

Endoscopy can be used to visualise oesophagitis but best avoided as requires GA so risk of further reflux

Oesophagoscopy also diagnostic of strictures

manometry and 24 hour pH measurement distal oesophagus

60
Q

Treatment of gastro-oesophageal reflux

A

Mild cases (e.g. overnight reflux) just sucralfate (as suspension not tablets) and low fat diet (fat predisposes to reflux as reduces GOS pressure and delays stomach emptying).

More severe cases: acid secretory inhibitors (e.g. H2 antagonists such as cimetidine) and prokinetics such as metoclopramide to increase GOS tone.

61
Q

Treatment of oesophagitis

A

EARLY AND AGGRESSIVE TREATMENT ESSENTIAL

Mucosal protectants
- sucralfate

Acid secretory inhibitors
- Cimetidine
- Ranitidine
- Famotidine
- Omeprazole

Drugs to increase the GOS tone and prevent further reflux
- metoclopramide

Analgesia

62
Q

Treatment of oesophageal stricture

A

treat oesophagitis first before dilating stricture

Stretch with bougies or a balloon catheter

Bougienage uses longitudinal forces and may be better for tough/fibrous strictures or v narrow strictures.

Balloon dilation: Balloon placed within stricture under ultrasound guidance. Radial forces.

After dilation, use anti-inflammatory doses of prednisolone

Diet: little and often high energy gruel.

63
Q

Hiatal hernia

A

Congenital or acquired, dogs and cats.

Sliding hiatal hernia commonest - GOS displaced into terminal oesophagus along with variable amount of rest of stomach

Rolling (para-oesophageal) hiatal hernia very rare in small animals

64
Q

Congenital hiatal hernia

A

Chinese shar-peis, English bulldogs and chow chows due to incomplete closure diaphragmatic hiatus.

Often present at weaning.

65
Q

Acquired hiatal hernias

A

secondary to increased intra-abdominal pressure with chronic vomiting

(including with inflammatory bowel disease in cats)

and also physiological during airway obstructions
e.g. laryngeal paralysis due to reduced intrathoracic pressure when inspiring.

66
Q

Clinical signs of hiatal hernia

A

May be asymptomatic or may be intermittent regurgitation due to oesophagitis caused by gastroesophageal reflux (GOS ineffective when herniated) ± vomiting due to mechanical obstruction of stomach - so history/signs can be confusing.

May also show dyspnoea if large hernia ± aspiration.

67
Q

Diagnosis of hiatal hernia

A

Plain ± contrast X-rays may show part of stomach ± rugal folds in caudodorsal thorax

Diagnosis hard if intermittent and must differentiate from caudal oesophageal/peri-oesophageal neoplasia on X-rays.

Fluoroscopy helpful ± oesophagoscopy for distal oesophagitis

68
Q

Treatment of hiatal hernia

A

Surgical correction often necessary in congenital form

Acquired hiatal hernias often managed successfully medically with sucralfate, gastric acid secretory inhibitors and low fat food and treatment of underlying cause.

Advice is to try medical management first and do surgery if that does not work.

69
Q

Oesophageal diverticulum

A

Uncommon.

Congenital and acquired.

70
Q

Congenital oesophageal diverticulum

A

bulldogs and shar-peis and usually a cranial thoracic “loop”.

71
Q

Acquired oesophageal diverticulum

A

Acquired divided into:

○ Pulsion (false) diverticulum: outpouching of mucosa through tear in muscularis. Presumed due to pressure within oesophagus e.g obstruction, regional peristaltic abnormalities. Usually just proximal to diaphragm.

○ Traction (true) diverticulum: all layers of oesophageal wall. Assumed due to traction from an external, adhesed fibrous band secondary to inflammation outside the oesophagus in airways, lungs, lymph nodes or pericardium.

72
Q

Diagnosis of oesophageal diverticulum

A

If small, may be no clinical signs and may go un-noticed.

If large ± multiple, see regurgitation ± aspiration pneumonia.

Radiography: may see diverticulum packed with ingesta on plain films.

Barium will outline diverticulum (± fluoroscopy ± oesophagoscopy).

Acquired often in distal high pressure zone and important to differentiate from mass or foreign body.

73
Q

Treatment of oesophageal diverticulum

A

Surgery if big/causing serious clinical problems.

Prognosis poor if large/multiple diverticula require resection.

74
Q

Peri-oesophageal masses

A

Uncommon.

Usually only partial obstruction so often regurgitate food but not fluids ± aspiration pneumonia ± develop megaoesophagus cranial to mass due to chronic obstruction.

If trachea ± cranial vena cava involved may also see respiratory signs ± oedema of head/fore-legs.

75
Q

Commonest causes of peri-oesophageal masses

A

Cervical oesophagus:
- carcinomas thyroid or larynx;
- salivary gland tumours;
- metastases e.g. of tonsillar carcinomas to cervical lymph nodes - abscesses or granulomas.

Thoracic oesophagus:
- cranial mediastinal lymphomas or thymomas;
- large lung tumours;
- heart base tumours
- abscesses/granulomas.

76
Q

Diagnosis of peri-oesophageal masses

A

Radiographs ± contrast ± ultrasound ± fine needle aspirates/biopsy especially if mediastinal.

Could also use oesophagoscopy to assess degree of infiltration of oesophageal wall if considering surgery.

77
Q

Oesophageal neoplasia

A

Very rare in dogs and cats, except in areas where Spirocerca (oesophageal worm) is endemic

Otherwise, commonest oesophageal tumours are metastases e.g from thyroid carcinoma.

Primaries include squamous cell carcinoma, leiomyomas which may involve the oesophageal-gastric junction and sarcomas.

78
Q

Treatment of oeosphageal neoplasia

A

surgery but prognosis poor unless “shell out” easily.

Some cases of Spirocerca have been reported to have secondary hypersialosis and to respond to phenbarbitone

79
Q

Gastro-oesophageal intussusception (GOI)

A

Rare.

May see intermittent GOI in dogs and especially cats secondary to chronic vomiting (similar to acquired hiatal hernias).

These cases respond to treatment of underlying cause and conservative therapy as described under hiatal hernia.

Most cases more catastrophic with marked intussusception causing vomiting, respiratory signs, shock and death in 95% - often secondary to oesophageal motility disorder e.g megaoesophagus.

Gastropexy indicated if diagnosed early enough.

80
Q

Dietary management of oesophageal disease

A

Small, frequent, highly digestible low-fat meals

Elevated food and water bowls or stairs

Optimal consistency varies for patients
○ Liquid: stricture/muscle weakness
○ Balls: Dysphagia
○ Firm: Sensory deficit

Keep patient upright for 5-10 minutes after eating

Gastrostomy tubes
○ Malnourished
○ Recurrent aspiration pneumonia

81
Q

Vomiting reflex

A

initiated by stimulating the vomiting centre in the medulla

vomiting centre can be stimulated directly, or indirectly via the chemoreceptor trigger zone (CRTZ)

Receptors: opioid, dopamine (D2), serotonin (5HT), neurokinin (NK-1), Histamine

Neurological input from the vestibular nucleus can also stimulate the CRTZ or the vomiting centre

82
Q

Nausea

A

Increased salivation and swallowing ± tachycardia.

Antiperistalsis of duodenum and jejunum and reduction in gastric tone (so note bile + SI content normal in vomitus)

83
Q

Retching

A

spasm of diaphragm, intercostal muscles and abdominal muscles to overcome distal oesophageal sphincter pressure

84
Q

Vomiting

A

distal oesophageal sphincter relaxes.

Food pushed out of relaxed stomach by action of abdominal and respiratory muscles

85
Q

Commonly selected anti-emetics

A

Metoclopramide

Maropitant

Ondansetron

86
Q

Metoclopramide

A

i.v. over 24 hours as slow constant rate infusion

D2 antagonist, 5-HT3 antagonist (weak), H1 antagonist (weak)

Central emetogenic pathway (D2 antagonism)

Variable prokinetic effect (peripheral)

Side effects include movement disorders, extrapyramidal signs

87
Q

Maropitant

A

Standard emesis

s.c. q24h.

For prevention of motion sickness up to 8mg/kg p.o. q24h for maximum of 2 days

NK1 receptor antagonists (highly selective)

Work well versus both peripheral and central emetogens

Use with caution in cardiac disease, hepatic disease, hypoproteinaemia and when administering other highly protein bound drugs

88
Q

Ondansetron

A

i.v. loading dose followed by infusion for 6 hours or p.o. q12-24 hours

5-HT3 selective antagonist

Works best versus acute peripheral emetogens (e.g. chemical irritants to the gut - cisplatin causing degranulation of enterochromaffin cells and 5-HT release).

Also effective vs. radiation induced emesis

Expensive and iv use only

89
Q

Normal gastric anatomy and function

A

Gastric pH about 1-1.5 during a meal

pH as high as 3-6.5 between meals

blood in vomit may appear either as coffee grounds or as fresh blood

Gastric mucosa protected from autodigestion by tight junctions between epithelia and rapid epithelial repair

Prostaglandins especially PGE2 important in controlling acid secretion

Many neurotransmitters involved in GI motility

normal gastric motility requires vagal inpu

90
Q

Normal gastric motility

A

Vagally-mediated gastric muscle

Normal mixing and breaking up of food particles - controlled via gastric pacemaker

Normal regulation of gastric emptying - ordered motility of the fundus, body and antrum

Fasting migrating motility complexes - slowly moving peristaltic waves

Signals from small and large intestine - generally acting to slow gastric emptying

91
Q

Gastric causes of vomiting

A

Gastritis

Ulceration

Neoplasia

Outflow obstruction

Foreign bodies

Motility/functional disorders

92
Q

Intestinal causes of vomiting

A

Inflammatory bowel disease

Neoplasia

Foreign bodies

Intussusception

Enteritis/enteropathy

Functional disorders

93
Q

Pancreatic causes of vomiting

A

Pancreatitis

Neoplasia

94
Q

Liver causes of vomiting

A

Hepatitis

Cholangitis

Biliary obstruction

Neoplasia

Abscess

95
Q

Splenic causes of vomiting

A

Mast cell tumour

96
Q

Genitourinary causes of vomiting

A

Nephritis

Pyelonephritis

Nephrolithiasis

Urinary obstruction

Pyometra

Neoplasia

Peritonitis

97
Q

Metabolic/endocrine causes of vomiting

A

Uraemia

DIabetic ketoacidosis

Hyperthyroidism

Hypoadrenocorticism

Hepatic encephalopathy

Hypercalcaemia

Septicaemia

98
Q

Drugs that can cause vomiting

A

IV medications

Digoxin

Chemotherapy

Xylazine

NSAID

99
Q

Toxic causes of vomiting

A

Lillies

Ethylene glycol

Lead

100
Q

Dietary causes of vomiting

A

Sudden change

Indiscretion

Intolerance

Allergy

101
Q

Neurologic causes of vomiting

A

Vestibular disease

Encephalitis

Neoplasia

Raised intracranial pressure

102
Q

Infectious causes of vomiting

A

Feline panleukopenia

Virulent calici

FIP

FeLV

FIV

Salmonellosis

Heartworm

103
Q

Predominant features of acute gastritis

A

Vomiting of sudden onset

104
Q

Predominant features of gastric ulceration or erosion

A

Vomiting

Haememesis

Melena

+/- anaemia

105
Q

Predominant features of gastric dilation/volvulus

A

Non-productive retching

Abdominal distension

Tachycardia

106
Q

Predominant features of chronic gastritis

A

Chronic vomiting of food or bile

107
Q

Predominant features of delayed gastric emptying

A

Acute to chronic vomiting more than 8 to 10 hours after feeding

108
Q

Predominant features of gastric neoplasia

A

Chronic vomiting

Weight loss

+/- anaemia

109
Q

Most common reasons for vomiting in cats

A

Chronic: idiopathic inflammatory gastritis or enteritis (IBD), adverse reactions to food, liver disease, uraemia

Hyperthyroidism

Hairballs

Linear foreign bodies

ALpha 2 adrenergic drugs

110
Q

Classic history of gastroduodenal reflux (bilious vomiting syndrome) in dogs

A

otherwise well dog vomits bile only in the mornings

111
Q

Cause of Gastroduodenal reflux = bilious vomiting syndrome

A

Prolonged contact between bile and gastric mucosa, resulting in mucosal damage (bile is detergent) and focal antral gastritis

Occurs in early morning because stomach is then empty so bile is not diluted by food +/- may be dysfunction of the duodeno-gastric area during sleep

112
Q

Diagnosis of bilious vomiting syndrome

A

Definitive diagnosis difficult: typical history, rule out other causes and response to treatment is usually enough.

May see antral gastritis on endoscopy +/- excessive bile retention

113
Q

Treatment of bilious vomiting syndrome

A

Split food in to multiple small feeds including last thing at night.

If no obvious gastritis, there is an argument to use increased fat in these dogs to delay gastric emptying.

Dietary management may be all that is necessary.

If diet alone ineffective, use promotility drugs e.g. metoclopramide to co-ordinate gastric and duodenal motility.

If significant concurrent gastritis, use gastric acid secretory inhibitors ± antacids ± sucralfate

114
Q

Central acute vomiting disorders (often acute, may be chronic)

A

Stimulation of chemoreceptor trigger zone e.g. apomorphine (dogs), cardiac glycosides, toxins (e.g. uraemia, liver disease, bacterial toxins), metabolic disorders (e.g ketoacidosis).

Stimulation of vomiting centre by CNS disease: neoplasia, inflammation, increased CSF pressure, epilepsy

Vestibular input in to vomiting centre (cats) or CRTZ (dogs)

Stimulation of vomiting centre by higher centres (fear, stress, pain)

115
Q

Gastric ± intestinal disease causing acute vomiting

A

Acute gastritis caused by dietary indiscretion/over-eating/sudden diet change

Toxins e.g. heavy metals, cardiac glycosides, metaldehyde, non-steroidal anti- inflammatory drugs, uraemia, erythromycin

Infections:
* Viral: canine parvovirus, canine adenovirus, canine distemper, feline panleucopenia, FIP
* Bacterial: leptospirosis, salmonella
* Parasitic: roundworms, hookworms (mainly young dogs/cats)

Gastric foreign body

Gastric dilatation/volvulus

Gastric motility disorders e.g. pylorospasm, gastroduodenal reflux

Small ± large intestinal foreign body / obstruction / volvulus / intussusception / inflammation

Haemorrhagic gastroenteritis (can be hard to differentiate from canine parvo virus)

116
Q

Extra-intestinal abdominal disease causing acute vomiting

A

Acute pancreatitis

Acute hepatitis

Acute renal disease / urinary tract obstruction / uraemia

Pyometritis

Peritonitis

117
Q

Metabolic / endocrine disease causing acute vomiting

A

Hypoadrenocorticism (“Addison’s disease” - dogs)

Hypokalaemia

Hypercalcaemia (e.g. malignancy, hyperparathyroidism)

Diabetic ketoacidosis

Hyperthyroidism (cats).

118
Q

Treatment of acute uncomplicated gastroenteritis

A

starve for 24-48 hours.

Water ± electrolytes only by mouth, followed by little and often feeding bland, low fat diet and gradual re-introduction of normal food after 7-10 days.

Drug therapy (including antibiotics) usually unnecessary - antibiotics may disrupt normal gut flora and predispose to small intestinal bacterial overgrowth.

119
Q

Lymphocytic-plasmacytic (superficial) gastritis

A

Lymphocytes and plasma cells± fibrosis in mucosa ± lamina propria

Tend to be systemically well + no gastric ulceration

120
Q

Eosinophilic gastritis

A

Sometimes associated peripheral eosinophilia, but inconsistent finding.

See diffuse eosinophilic infiltrate of mucosa or full thickness focal eosinophilic granulomas (which may look grossly neoplastic)

Tend to be systemically ill with gastric ulceration

121
Q

Atrophic gastritis

A

thin mucosa with reduced glands.

Rare.

Parietal cells become mucus secreting, so should be achlorhydria (reduced gastric acidity) but poorly documented in animals

Tend to be systemically well + no gastric ulceration

122
Q

Hypertrophic gastritis

A

Grossly thickened mucosa/rugal folds.

May be diffuse or focal (e.g. around pylorus causing acquired pyloric stenosis).

On histology, see mucosal epithelial and/or glandular hypertrophy ± variable inflammatory cell infiltrate

Tend to be systemically ill with gastric ulceration

123
Q

Chronic gastritits

A

Commonest are lymphocytic-plasmacytic and eosinophilic gastritis

may affect just the stomach or SI ± LI or be generalised

“Endoscopic patch testing” - to test for food allergy

Inflammation in hypertrophic and eosinophilic forms may be severe enough to result in hypoproteinaemia

Eosinophilic gastritis or gastroenteritis associated with endoparasite infection in some cases

Hypertrophic gastritis thought to result from chronic increase in gastric trophic factors

124
Q

Food sensitivity vs IBD

A

Food responsive GI disease will resolve completely when offending food is removed from the diet, and recur if rechallenged

Biopsies tend to be unremarkable

Although the exact aetiology of IBD is unknown it is considered a multifactorial disease with the mucosal immune system, microbiota, environment, and genetics all playing a role

125
Q

Diagnosis of chronic gastritis

A

chronic vomiting ± systemically unwell,

diarrhoea is probably a more common clinical sign;

contrast radiography ± ultrasound wall thickening but normal layers;

bloods show protein-losing gastropathy only if severe;

endoscopic or surgical biopsy definitive.

Contrast radiographs with hypertrophic gastritis may show changes typical of pyloric stenosis.

126
Q

Treatment of chronic gastritis

A

Diet: starvation not appropriate in chronic gastric disease. Home-made novel protein source diet if inflammatory infiltrate + little and often

Gastric acid secretory inhibitors indicated in all cases. If obvious ulceration, sucralfate as well.

Effective endoparasite control, particularly if eosinophilic gastritis

Consider promotility drugs e.g. metoclopramide, ranitidine

Consider antibiotics for probable small intestinal bacterial overgrowth (oxytetracycline or metronidazole or tylosin)

Surgery if hypertrophy with acquired pyloric stenosis

If above medical therapies not effective alone, add in anti-inflammatory doses of prednisolone for lymphocytic-plasmacytic, immunosuppressive doses for eosinophilic gastritis

127
Q

Causes of gastric ulceration

A

NSAIDs

Steroids

Uraemia/renal failure

Liver disease

128
Q

NSAID induced gastric ulceration

A

Direct mucosal injury (“Ion-trapping”).

Inhibit PG synthesis so reduce gastric mucus and bicarbonate secretion, increase acid secretion and may reduce mucosal cell turnover.

Ion-trapping occurs when NSAIDs move into GI epithelial cells and are ionized so that they are now not lipophilic and can’t move across membranes.

129
Q

Steroid induced gastric ulceration

A

rarely ulcerogenic alone.

Reduce mucosal cell renewal and PG synthesis so reduce mucus and increase acid secretion

130
Q

Uraemia/renal failure induced gastric ulceration

A

Ammonia toxic to gastric mucosa;

Reduced metabolism of gastrin;

Reduced gastric blood flow

131
Q

Liver disease induced gastric ulceration

A

Portal hypertension causes ischaemia of gut wall and reduced epithelial cell turnover, reduced mucus

132
Q

Diagnosis of gastric ulceration

A

haematemesis + melaena ± anaemia (may be iron deficiency if chronic);

systemically unwell;

contrast radiography;

ultrasonography;

gastroscopy + biopsy.

133
Q

Treatment of gastric ulceration

A

usually treat for 2-3 weeks

Treat underlying disease

AGGRESSIVE DRUG TREATMENT IMPORTANT - potential for severe blood loss ± ulcer erosion and peritonitis.

Gatric secretory inhibitors
- cimetidine
- ranitidine

Proton pump inhibitors
- omeprazole

Sucralfate

DO NOT STARVE

134
Q

Causes of pyloric outflow obstruction

A

Gastric FB

Congenital pyloric stenosis

Acquired pyloric stenosis

Gastroduodenal intussusception

135
Q

Pyloric foreign body

A

Commonest cause of pyloric outflow obstruction.

Usually intermittent clinical signs caused by foreign body moving in and out of the pyloric antrum.

136
Q

Congenital pyloric stenosis

A

Muscular hypertrophy obstructs pyloric outflow.

Rare.

Brachycephalics e.g. boxers, boston terriers.

Also recognised in Siamese cats in combination with megaoesophagus.

137
Q

Acquired pyloric stenosis

A

May be the result of external compression or may be due to gastric lesion blocking pyloric antrum

Uncommon syndrome of acquired antral pyloric mucosal hypertrophy in middle-aged to old small breed dogs.

Marked mucosal hypertrophy/folds but muscle remains normal.

Cause unclear - may be increased trophic factors (as hypertrophic gastritis) and as particularly affects small, excitable breeds, perhaps related to chronic stress/pylorospasm.

138
Q

Gastroduodenal intussusception

A

Also causes pyloric outflow obstruction.

Very rare - only one case report in a dog and a few in man.

Can be intermittent.

139
Q

Gastric motility disorders

A

Mechanical obstruction e.g. pyloric stenosis or foreign body

Functional obstruction: delayed gastric emptying

Gastroduodenal reflux = bilious vomiting syndrome

Gastric dilatation-volvulus

140
Q

Treatment of mechanical gastric obstructions

A

Treatment usually surgical

USE OF PROKINETICS CONTRA-INDICATED

141
Q

Gastric dilatation-volvulus

A

MEDICAL AND SURGICAL EMERGENCY

Usually large, deep-chested dogs.

Primary cause poorly understood

142
Q

Gastric neoplasia

A

Benign tumours more common than malignant in dogs - leiomyomas and polyps

Benign gastric tumours v. rare in cats

Malignant gastric tumours = 1% of all tumours in the dog and less in cat.
Usually middle-aged to old.
Adenocarcinomas commonest in dogs.
Lymphosarcomas, fibrosarcomas and leimyosarcomas and gastric metastases are much less common

143
Q

Dog breeds that are pre-disposed to pancreatitis

A

Miniature schnauzers

Cocker spaniels

Cavalier King Charles spaniels

Terrier breeds

Border collies

144
Q

Diagnosis of pancreatitis

A

Need to correlate painful episodes and vomiting with pancreatic enzyme elevations

145
Q

Metabolic causes of vomiting

A

include renal and hepatic disease as well as numerous endocrinopathies

This emphasizes the importance of blood biochemical analysis before moving on to more focused GI testing

SA Alimentary (37 decks)

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