vomiting, regurgitation, dysphagia Flashcards
what is the physiology of vomiting?
Vomiting is an active reflex mediated via the emetic centre that can be stimulated via the chemoreceptor trigger zone (CRTZ) or GI tract, 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 vomiting there are several systems to consider as possible causes.
what is the pathophysiology of regurgitation? what are yopu thinging about with regugitation in terms of causes?
- Passive expulsion of food from the pharynx or oesophagus.
◦ doesn’t make much noise,
◦ can be silent regurgitation - nothing comes out, they chew and swallow again - This is a failure of swallowing (Dysphagia) and/or subsequent movement of food down the oesophagus to the stomach.
- Realistically we should therefore be considering anatomy, particularly muscular and neurological systems involved in eating and swallowing.
- Oesophagus – proximal and distal sphincters, food moves between them via peristalsis, controlled by the muscular wall (dogs – striated, cats – striated proximally and smooth distally)
what are the causes of dysphagia?
Failure to prehend/bite (mouth) and initially swallow (pharynx):
- Pain – on closing (e.g. dental disease, stomatitis) or on opening (e.g. retrobulbar abscess) or both (fractured jaw, TMJ disease).
- Failure of neuro-muscular control – cranial nerves disease (V, VII, IX, X, XII), CNS disease, masticatory myositis, Botulism, myasthenia gravis.
- Obstruction – pharyngeal FB, polyp, neoplasia, abscessation, lymphadenopathy
what are the causes for regurgitation?
Failure to pass the oesophagus:
* 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), mural (wall) or extramural (external)
◦ Intraluminal – foreign body, stricture (e.g. secondary to oesophagitis)
◦ Mural – neoplasia, inflammation
◦ Extramural – Vascular ring anomaly, Hiatal Hernia, SOL (neoplasia)
* ** Neuro-muscular disorder** – Myasthenia gravis, botulism, tetanus, distemper, dysautonomia, peripheral neuropathy (e.g. autoimmune), Addisons, Hypothyroidism
what pateitns is vomiting an emergency?
collapsed, poorly responsive, signs of hypovolaemia, etc and proceed to triage if the case.
why is it important to assess BCS with a vomitng patient?
why is it important to check head muscles with a dyphagic patient?
why is it important to assess neuro function with a vomitng patient?
why is it important to assess recent medical history with a vomitng patient?
- Body condition score to assess for true acute vs chronic but missed by the owners.
- Muscle quality e.g. masticatory muscles to look for reasongs why dysphagic (masticatory myositis, trigeminal nerve damage.)
- Neurological abnormalities – behavioural changes, ataxia, cranial nerve deficits, exhaustible blink etc.
- Recent medical history – aspiration risk in surgery causing oesophagitis, or medications e.g. doxycycline and risk of oesophagitis.
signalment clues:
what signalment is assocatied with each of these?
* Congenital megaoesophagus
* Congenital and acquired
* Vascular ring anomaly – persistent right aortic arch
* Intussusception
- Oesophageal foreign body
- Myasthenia gravis
- Gastric/intestinal foreign bodies
- Doxycycline induced oesophagitis
- Neoplasia
- Congenital megaoesophagus – Labrador, Newfoundland, Shar-Pei
- Congenital and acquired – Great Dane, GSD, Irish Setters.
- Vascular ring anomaly – persistent right aortic arch GSD, Irish setter, Great Dane
- Intussusception – Juvenile, puppies with recent diarrhoea. - needs surgery quickly
- Oesophageal foreign body – terrier breeds (particularly WHWT!) and spaniels (lamb bones)
- Myasthenia gravis – GSD, Golden retriever, GSP
- Gastric/intestinal foreign bodies – Labradors, Spaniels
- Doxycycline induced oesophagitis – cats (need to make sure to they eat with drug)
- Neoplasia – older animals
what diagnostic test can be done for vomiting, regurgataion and dysphagia?
This depends on what your suspicious of!
* Imaging – primarily looking for obstructive/anatomical disease
◦ Radiography - (L5/SI ratio > 1.7, a ratio <1.7 does not rule out obstructive disease)
◦ Ultrasound – operator dependant, don’t forget POCUS for free fluid!
‣ worried about perforation of the intestine that has caused free fluid
◦ (CT/fluoroscopy)
- Direct Visualisation – Examination under GA, Endoscopy – Upper GI foreign bodies, inflammatory disease – biopsy opportunity.
Look for systemic/metabolic diseases – Haematology/Biochemistry
Specific blood tests – e.g. cPLI (Pancreatitis, inflammation of the pancrease, can be causes by many things)), AChR (M. Gravis), basal cortisol (Addisons), T4/TSH (HypoT4)
what is the initial management if abnormal swallowing?
Trial and error to find the food type tolerated – may require a feeding tube in the short term to stabilise.
what is the inital management of regurgitation: think abotu the different causes?
Megaoesophagus - Difficult to manage!
* Omeprazole (PPI) – risk of aspiration that could lead to aspiration pneumonitis . (proton pump inhibitors, reduces acid secretions)
* Feed from a height – 5-10 minutes! Small balls rather than big amounts. Could consider a feeding tube. Prognosis is often poor for chronic regurgitation.
* Treat any concurrent/underlying disease e.g. hypothyroidism, PRAA, etc.
Oesophagitis – Pain relief!! Feeding Tube (bypass the oesophagus)
Oesophageal Foreign body – remove it, endoscopy, consider referral – rupture -> thoracotomy
name three antiemetics and how they work
- Maropitant – NK1 antagonist -> helps with centrally mediated vomiting e.g. metabolic, CRTZ, Vestibular
- Metoclop – D2 receptor antagonist and 5-HT3 receptor antagonist -> Dual effect, CRTZ and lower oesophageal sphincter, BUT prokinetic so if FB present could rupture the GI Tract
- Ondansetron – 5HT3 – centrally acting (CRTZ) – very effective at reducing nausea (expensive and off licence, third line)
what can you do in vomiting cases where BCS is reducing?
- Consider feeding tubes – bypass the problem if you can; NO/NG tube, O tube, PEG tube.
- TPN/PPN – parenteral nutrition; ideally a central line is required so not often a routine first opinion approach but it is feasible with good nursing.
name 4 gastroprotectants and how they work?
-
Omeprazole – Proton Pump Inhibitor, reduced H+ secretion -> useful for gastric ulceration (and reducing CSF production e.g. Syringomyelia). Long term use -> Dysbiosis. < 3-4 weeks.
◦ still need to find the underlying cause of the ulcer - Misoprostol – Prostaglandin analogue – Increases mucosal blood flow and therefore healing e.g. ulcers – DON’T USE IN PREGNANCY – primarily used for NSAID tox
- H2 Receptor antagonists e.g. cimetidine – reduce acid secretion, effectiveness is questionable, minimal research in small animal and not supportive.
- Sucralfate – polyionic surfactant (anion) binds to damaged mucosa (positively charged proteins exposed) – weak evidence for use in oesophagitis, probably not helpful in gastric ulceration – use liquid not tablets.
what disease do you need to consider with a regurgitating BOAS dog?
what is occuring?
how is it diagnosed? and treated?
Hiatal hernia
particularly French Bulldogs
The oesophagus passes through the hiatus of the diaphragm, normally they are well attached and both travel forwards and backwards as the patient breathes. In a HH, the diaphragm and oesophagus are poorly attached, as the patient breathes the diaphragm ‘slides’ over the oesophagus and allows the cranial part of the stomach to herniate into the chest -> Gastro-oesophageal reflux.
Diagnosis is difficult on radiography as it’s a real time problem, so fluoroscopy is better. Treatment is surgical repair, realistically, referral.
whast type of hernia is more common in cats and has a genetic basis, often found incidentally?
PPDH – pericardio-peritoneal diaphragmatic hernia
A midline defect at birth, which allows abdominal contents to herniate into the pericardial sac! Often found incidentally rather than as a result of any clinical illness.
