Approach to vomiting, regurgitation & dysphagia Flashcards
(24 cards)
V+ - physiology
- v+ is an active reflex mediated via the emetic centre that can be stimulated via the chemoreceptor trigger zone (CRTZ) or GIT, cerebral cortex, or vestibular system
- the CRTZ is full of various receptors and samples the blood for endogenous (e.g. azotaemia - renal, ammonia - hepatic, inflammatory mediators) or exogenous (e.g. drugs/toxins) substances
- this means in v+ there are several systems to consider as possible causes
Acute vs chronic v+
- acute is more likely to be toxic, obstructive, inflammatory, infectious
- chronic is more likely to be chronic inflammatory, chronic infectious, metabolic/endocrine, neoplastic
- but there is always cross over
Acute v+ - causes
GIT
- obstructive (FB, neoplasia, parasitic, constipation, intussusception, volvulus)
- inflammatory (gastritis, gastroenteritis, colitis)
- mucosal insult (dietary indiscretion, intolerance, sudden change in diet, toxins)
- infectious (bacterial/viral/parasitic)
- gastric stretch (i.e. ate too much)
- visceral pain
Cerebral cortex
- head trauma
- sudden changes in ICP
Vestibular system
- motion sickness
- idiopathic vestibular dz
- otitis interna
CRTZ
- endogenous
– any systemic metabolic or endocrine dz resulting in acute changes
– e.g. DKA, Addisons, AKI, pancreatitis, acute hepatitis, peritonitis, prostatitis, pyometra, electrolyte disturbances, acid-base disturbances
- exogenous
– toxins/drugs
Chronic v+ - causes
GIT
- chronic inflammatory (gastritis, gastroenteritis, colitis, chronic enteropathy)
- mucosal insult (dietary intolerance)
- infectious (bacterial/viral/parasitic)
- obstructive (pyloric FB, neoplasia, parasitic, constipation
Cerebral cortex
- neoplasia/SOL
- CNS dz
Vestibular system
- chronic vestibular damage
- otitis interna
- neoplasia
- cerebellar dz
CRTZ
- endogenous
– any systemic metabolic or endocrine dz resulting in chronic changes
– e.g. DM, Addison’s, CRF, liver failure, chronic pancreatitis, electrolyte disturbances, acid-base disturbances, hyperthyroidism (cats)
- exogenous
– toxins/drugs less likely
Regurgitation (& dysphagia) - physiology
- passive expulsion of food from the pharynx or oesophagus
- failure of swallowing (dysphagia) and/or subsequent movement of food down the oesophagus to the stomach
- therefore consider anatomy, particularly muscular and neurological systems involved in eating and swallowing
- oesophagus
– proximal & distal sphincters
– food moves between them via peristalsis
– controlled by muscular wall (dogs - striated, cats - striated proximally and smooth distally)
What is dysphagia?
- failure to prehend/bite (mouth) and initially swallow (pharynx)
Dysphagia - causes
Pain
- on closing e.g. dental dz, stomatitis
- on opening e.g. retrobulbar abscess
- or both e.g. fractured jaw, TMJ dz
Failure of neuromuscular control
- CN dz (V, VII, IX, X, XII)
- CNS dz
- masticatory myositis
- botulism
- myasthenia gravis
Obstruction
- pharyngeal FB
- polyp
- neoplasia
- abscessation
- lymphadenopathy
Regurgitation - causes
Dilatation (megaoesophagus)
- may be congenital or occurring via either being active stretch (e.g. a chronic obstruction) or passive stretch (weak muscular wall, dysmotility) or idiopathic
Obstruction
- intraluminal (internal) e.g. FB, stricture (e.g. secondary to oesophagitis)
- mural (wall) e.g. neoplasia, inflammation
- extramural (external) e.g. vascular ring anomaly (remnant tissue clamping down the oesophagus where it passes the mainstem aorta), hiatal hernia, SOL (neoplasia)
Neuromuscular disorder
- myasthenia gravis
- botulism
- tetanus
- distemper
- dysautonomia
- peripheral neuropathy e.g. autoimmune
- Addisons
- hypothyroidism
How to differentiate v+ with regurgitation/dysphagia
V+
- active
- usually associated with retching, abdominal effort and lots of noise
Regurgitation
- passive
- food just plops out
- no retching
- less noise
Hx & CE
In the v+ pt determine if they are an emergency i.e. collapsed, poorly responsive, signs of hypovolaemia, etc.
Recent medical hx
- aspiration risk in sx for oesophagitis
- meds e.g. doxycycline and risk of oesophagitis
GI dz
- diet change
- scavenging
- FB risk
- access to toxins
- worming regime
- d+
- constipation
Neuro abnormalities
- behavioural changes
- ataxia
- CN deficits
- exhaustible blink
Pain
BCS
- to asses for true acute vs chronic missed by O
Muscle quality
- e.g. masticatory muscles
Signs of systemic dz
- e.g. PUPD, jaundice
Signalment clues - congenital megaoesophagus
- labs
- Newfoundland
- Shar-Pei
Signalment clues - congenital & acquired megaoesphagus
- great dane
- GSD
- Irish setters
Signalment clues - vascular ring anomaly (persistent right aortic arch)
- GSD
- Irish setter
- Great Dane
Signalment clues - intussusception
- juvenile
- puppies with recent d+
Signalment clues - oesophageal FB
- terrier breeds (esp WHWT)
- spaniels (lamb bones)
Signalment clues - myasthenia gravis
- GSD
- GRet
- GSP
Signalment clues - gastric/intestinal FB
- labs
- spaniels
Signalment clues - doxycycline induced oesophagitis
- cats
Signalment clues - neoplasia
- older animals
Diagnostic testing options
Imaging - primarily looking for obstructive/anatomical dz
- radiography
- US + POCUS
- (CT/fluoroscopy)
Direct visualisation
- endoscopy under GA: upper GI FB, inflammatory dz, biopsy opportunity
Look for systemic/metabolic dz
- haem
- biochem
Specific blood tests
- cPLI (pancreatitis)
- AChR (M. Gravis)
- basal cortisol (Addisons)
- T4/TSH (hypothyroidism)
Initial management / 1st aid - abnormal swallowing
- trial and error to find the food type tolerated
- may require a feeding tube in the short term to stabilise
Initial management / 1st aid - regurgitation
Depends on the cause
Megaoesophagus
- omeprazole (PPI): risk of worsened aspiration
- feed from the height: 5-10mins, small balls instead of big amount
- could consider a feeding tube
- prognosis is often poor for chronic regurgitation
- tx any concurrent/underlying dz e.g. hypothyroidism, PRAA
Oesophagitis
- pain relief (methadone/ket/fentanyl)
- feeding tube (bypass the oesophagus)
Oesophageal GB
- remove it
- endoscopy
- consider referral
- rupture -> thoracotomy
Initial management / 1st aid - v+
Consider the cause and tx the underlying
Be aware - reaching for drugs may mask the problem e.g. FB
Maropitant
- NK1 antagonist
- helps with centrally mediated v+ e.g. metabolic, CRTZ, vestibular
Metoclopramide
- D2 receptor antagonist and 5-HT3 receptor antagonist
- dual effect, CRTZ and low oesophageal sphincter
- but pro kinetic so if FB present could rupture the GIT
Ondansetron
- 5HT3 receptor antagonist
- centrally acting (CRTZ)
- very effective at reducing nausea
- expensive
- no license so probs 3rd line product
Nutrition
- esp in chronic cases when BCS is reducing
- consider feeding tubes: bypass the problem if you can
- TPN/PPN: parenteral nutrition; ideally a central line is required so not often a routine 1st opinion approach but it is feasible with good nursing
Initial management / 1st aid - Gastroprotectants
Omeprazole
- proton pump inhibitor
- reduced H+ secretion
- useful for gastric ulceration (and reducing CSF production e.g. Syringomyelia)
- long term use -> dysbiosis
- <3-4w
Misoprostol
- prostaglandin analogue
- increases mucosal blood flow and therefore healing e.g. ulcers
- DO NOT use in pregnancy
- primarily used for NSAID toxicity
H2 receptor antagonists
- e.g. cimetidine
- reduce acid secretion
- effectiveness is questionable
- minimal research in small animal and not supportive
Sucralfate
- polytonic surfactant (anion) binds to damaged mucosa (positively charged proteins exposed)
- weak evidence for use in oesophagitis
- probs not helpful in gastric ulceration
- use liquid not tablets
