Regurgitation and vomiting Flashcards
What clinical features in the dog or cat make you think it has oropharyngeal dysphagia?
Hunger with multiple messy attempts to eat
Pharyngeal retching
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.
Regurgitation
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
True vomiting
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
Congenital abnormalities that could cause vomtining/regurgitation
Vascular ring anomaly
Oesophageal diverticulum
Broncho-oesophageal fistula
Hiatal hernia
Most common dog breed to get foreign body in the oesophagus
West highland white terrier
Which breeds are overrepresented for regurgitation and hiatal hernia?
Brachycephalic dogs
What disorder could be worse when ingesting liquid?
pharyngeal dysphagia
Which disorders could be worse when ingesting food (rather than liquid)?
crichophalangeal achalasia
oesophagitis
What could cause gas in the oesophagus on radiograph?
Megaoesophagus
Vascular ring anomaly
Stricture
Severe oesophagitis
Aerophagia
What can cause aerophagia?
Excitement
Nausea
Anaesthesia/GA
Dyspnoea
Innervation of the pharynx
IX and X sensory and motor
Anatomy of oesophagus (layers)
mucosa, submucosa with mucous glands, muscularis + loose connective tissue (no serosa)
Canine muscularis muscle of the oesophagus
Two intertwining layers of striated muscle
Feline muscularis muscle of the oesophagus
Cranial and middle sections mixed smooth and striated
terminal 35% entirely smooth muscle
Upper oesophageal sphincter
cricopharyngeal sphincter (cricopharyngeal and thyropharyngeal muscles).
Relaxation co-ordinated with swallowing.
Prevents aerophagia and reflux of food from oesophagus into pharynx
Lower oesophageal sphincter
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).
Swallowing
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
Differential diagnoses of pharyngeal retching/dysphagia
Oropharyngeal trauma
Oropharyngeal foreign body
Oropharyngeal inflammation
Oropharyngeal mass
Salivary mucocoele, polyp, abscess
Neurological and muscular problems
Oropharyngeal trauma
Mandible
Maxilla
TMJ
Hyoid bones
Soft tissue
Oropharyngeal inflammation
Gingivitis
Stomatitis
Pharyngitis
Tonsillitis
Oropharyngeal masses
Tonsillar squamous cell carcinoma
Peripharyngeal lymphoma
Neurological and muscular problems leading to pharyngeal retching or dysphagia
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
Cricopharyngeal achalasia
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.
Clinical signs of cricopharyngeal achalasia
Severe dysphagia
Distress
Rhinitis
Aspiration
Weight loss
Often anorexia
Diagnosis of cricopharyngeal achalasia
History
Fluoroscopy during barium swallow
+/- manometry muscle
Treatment of cricopharyngeal achalasia
No successful medical treatment
Cricopharyngeal myotomy often curative
Important to differntiate from pharyngeal dysphagia as myotomy makes pharyngeal dysphagia worse
Pharyngeal dysplasia
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!).
Clinical signs of pharyngeal dysphagia
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.
Treatment of pharyngeal dysphagia
No treatment for idiophathic
Cricopharyngeal myopathy makes it worse
Idiopathic hypersialosis
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).
Anatomical differential diagnoses of regurgitation
Vascular ring anomaly
Hiatal hernia
Oesophageal diverticulum
Broncho-oesophageal fistula
Differential diagnoses for oesophagitis causing regurgitation
Trauma
Reflux (GA, Hiatal hernia, poor sphincter function)
Irritant (drugs, dietary indiscretion)
Secondary to megaoesophagus
Neuromuscular causes of regurgitation
Idiopathic megaoesophagus
myasthenia gravis,
myositis,
myopathy,
neuritis,
peripheral neuropathy,
central (brainstem disorders),
hypothyroidism,
hypoadrenocorticism,
toxicity (lead, thallium, anticholinesterase),
dysautonomia,
Sialoadenosis
Obstructive causes of regurgitation
Oesophageal foreign body (FB)
Oesophageal stricture
Gastroesophageal intussusception
Oesophageal and peri-oesophageal masses
Oesphageal mural neoplasia
Oesophageal foreign body signalment
Most common in terriers, particularly Westies
Oesophageal foreign body
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
Diagnosis of oesophageal foreign body
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
Treatment of oesophageal foreign body
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.
Oesophageal strictures secondary to oesophagitis
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
Megaoesophagus
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)
Congenital megaoesophagus
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.
Acquired megaoesophagus
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
Diagnosis of megaoesophagus
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).
Treatment of megaoesophagus
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
Gastro-oesophageal reflux/oesophageal hypomotility
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
Vascular ring anomaly incidence
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.
Possible vascular ring anomalies
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.
VRA and megaoesophagus
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.
Diagnosis of vasucalr ring anomalies
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
Vascular ring anomalies on plain radiographs
Dilated cranial thoracic oesophagus and ventral deviation of the trachea
Contrast studies with vascular ring anomalies
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
Treatment of vascular ring anomalies
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.
Gastro-oesophageal reflux
occurs when there is temporary or permanent gastroesophageal sphincter (GOS) incompetence
Results in oesophagitis
Causes of gastro-oesophageal reflux
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.
Gastro-oesophageal reflux under GA
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.
Oesophagitis
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.
Oesophageal stricture
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.
Diagnosis of Gastroesophageal reflux, oesophagitis and oesophageal stricture
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
Treatment of gastro-oesophageal reflux
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.
Treatment of oesophagitis
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
Treatment of oesophageal stricture
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.
Hiatal hernia
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
Congenital hiatal hernia
Chinese shar-peis, English bulldogs and chow chows due to incomplete closure diaphragmatic hiatus.
Often present at weaning.
Acquired hiatal hernias
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.
Clinical signs of hiatal hernia
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.
Diagnosis of hiatal hernia
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
Treatment of hiatal hernia
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.
Oesophageal diverticulum
Uncommon.
Congenital and acquired.
Congenital oesophageal diverticulum
bulldogs and shar-peis and usually a cranial thoracic “loop”.
Acquired oesophageal diverticulum
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.
Diagnosis of oesophageal diverticulum
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.
Treatment of oesophageal diverticulum
Surgery if big/causing serious clinical problems.
Prognosis poor if large/multiple diverticula require resection.
Peri-oesophageal masses
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.
Commonest causes of peri-oesophageal masses
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.
Diagnosis of peri-oesophageal masses
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.
Oesophageal neoplasia
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.
Treatment of oeosphageal neoplasia
surgery but prognosis poor unless “shell out” easily.
Some cases of Spirocerca have been reported to have secondary hypersialosis and to respond to phenbarbitone
Gastro-oesophageal intussusception (GOI)
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.
Dietary management of oesophageal disease
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
Vomiting reflex
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
Nausea
Increased salivation and swallowing ± tachycardia.
Antiperistalsis of duodenum and jejunum and reduction in gastric tone (so note bile + SI content normal in vomitus)
Retching
spasm of diaphragm, intercostal muscles and abdominal muscles to overcome distal oesophageal sphincter pressure
Vomiting
distal oesophageal sphincter relaxes.
Food pushed out of relaxed stomach by action of abdominal and respiratory muscles
Commonly selected anti-emetics
Metoclopramide
Maropitant
Ondansetron
Metoclopramide
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
Maropitant
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
Ondansetron
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
Normal gastric anatomy and function
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
Normal gastric motility
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
Gastric causes of vomiting
Gastritis
Ulceration
Neoplasia
Outflow obstruction
Foreign bodies
Motility/functional disorders
Intestinal causes of vomiting
Inflammatory bowel disease
Neoplasia
Foreign bodies
Intussusception
Enteritis/enteropathy
Functional disorders
Pancreatic causes of vomiting
Pancreatitis
Neoplasia
Liver causes of vomiting
Hepatitis
Cholangitis
Biliary obstruction
Neoplasia
Abscess
Splenic causes of vomiting
Mast cell tumour
Genitourinary causes of vomiting
Nephritis
Pyelonephritis
Nephrolithiasis
Urinary obstruction
Pyometra
Neoplasia
Peritonitis
Metabolic/endocrine causes of vomiting
Uraemia
DIabetic ketoacidosis
Hyperthyroidism
Hypoadrenocorticism
Hepatic encephalopathy
Hypercalcaemia
Septicaemia
Drugs that can cause vomiting
IV medications
Digoxin
Chemotherapy
Xylazine
NSAID
Toxic causes of vomiting
Lillies
Ethylene glycol
Lead
Dietary causes of vomiting
Sudden change
Indiscretion
Intolerance
Allergy
Neurologic causes of vomiting
Vestibular disease
Encephalitis
Neoplasia
Raised intracranial pressure
Infectious causes of vomiting
Feline panleukopenia
Virulent calici
FIP
FeLV
FIV
Salmonellosis
Heartworm
Predominant features of acute gastritis
Vomiting of sudden onset
Predominant features of gastric ulceration or erosion
Vomiting
Haememesis
Melena
+/- anaemia
Predominant features of gastric dilation/volvulus
Non-productive retching
Abdominal distension
Tachycardia
Predominant features of chronic gastritis
Chronic vomiting of food or bile
Predominant features of delayed gastric emptying
Acute to chronic vomiting more than 8 to 10 hours after feeding
Predominant features of gastric neoplasia
Chronic vomiting
Weight loss
+/- anaemia
Most common reasons for vomiting in cats
Chronic: idiopathic inflammatory gastritis or enteritis (IBD), adverse reactions to food, liver disease, uraemia
Hyperthyroidism
Hairballs
Linear foreign bodies
ALpha 2 adrenergic drugs
Classic history of gastroduodenal reflux (bilious vomiting syndrome) in dogs
otherwise well dog vomits bile only in the mornings
Cause of Gastroduodenal reflux = bilious vomiting syndrome
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
Diagnosis of bilious vomiting syndrome
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
Treatment of bilious vomiting syndrome
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
Central acute vomiting disorders (often acute, may be chronic)
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)
Gastric ± intestinal disease causing acute vomiting
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)
Extra-intestinal abdominal disease causing acute vomiting
Acute pancreatitis
Acute hepatitis
Acute renal disease / urinary tract obstruction / uraemia
Pyometritis
Peritonitis
Metabolic / endocrine disease causing acute vomiting
Hypoadrenocorticism (“Addison’s disease” - dogs)
Hypokalaemia
Hypercalcaemia (e.g. malignancy, hyperparathyroidism)
Diabetic ketoacidosis
Hyperthyroidism (cats).
Treatment of acute uncomplicated gastroenteritis
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.
Lymphocytic-plasmacytic (superficial) gastritis
Lymphocytes and plasma cells± fibrosis in mucosa ± lamina propria
Tend to be systemically well + no gastric ulceration
Eosinophilic gastritis
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
Atrophic gastritis
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
Hypertrophic gastritis
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
Chronic gastritits
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
Food sensitivity vs IBD
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
Diagnosis of chronic gastritis
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.
Treatment of chronic gastritis
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
Causes of gastric ulceration
NSAIDs
Steroids
Uraemia/renal failure
Liver disease
NSAID induced gastric ulceration
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.
Steroid induced gastric ulceration
rarely ulcerogenic alone.
Reduce mucosal cell renewal and PG synthesis so reduce mucus and increase acid secretion
Uraemia/renal failure induced gastric ulceration
Ammonia toxic to gastric mucosa;
Reduced metabolism of gastrin;
Reduced gastric blood flow
Liver disease induced gastric ulceration
Portal hypertension causes ischaemia of gut wall and reduced epithelial cell turnover, reduced mucus
Diagnosis of gastric ulceration
haematemesis + melaena ± anaemia (may be iron deficiency if chronic);
systemically unwell;
contrast radiography;
ultrasonography;
gastroscopy + biopsy.
Treatment of gastric ulceration
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
Causes of pyloric outflow obstruction
Gastric FB
Congenital pyloric stenosis
Acquired pyloric stenosis
Gastroduodenal intussusception
Pyloric foreign body
Commonest cause of pyloric outflow obstruction.
Usually intermittent clinical signs caused by foreign body moving in and out of the pyloric antrum.
Congenital pyloric stenosis
Muscular hypertrophy obstructs pyloric outflow.
Rare.
Brachycephalics e.g. boxers, boston terriers.
Also recognised in Siamese cats in combination with megaoesophagus.
Acquired pyloric stenosis
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.
Gastroduodenal intussusception
Also causes pyloric outflow obstruction.
Very rare - only one case report in a dog and a few in man.
Can be intermittent.
Gastric motility disorders
Mechanical obstruction e.g. pyloric stenosis or foreign body
Functional obstruction: delayed gastric emptying
Gastroduodenal reflux = bilious vomiting syndrome
Gastric dilatation-volvulus
Treatment of mechanical gastric obstructions
Treatment usually surgical
USE OF PROKINETICS CONTRA-INDICATED
Gastric dilatation-volvulus
MEDICAL AND SURGICAL EMERGENCY
Usually large, deep-chested dogs.
Primary cause poorly understood
Gastric neoplasia
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
Dog breeds that are pre-disposed to pancreatitis
Miniature schnauzers
Cocker spaniels
Cavalier King Charles spaniels
Terrier breeds
Border collies
Diagnosis of pancreatitis
Need to correlate painful episodes and vomiting with pancreatic enzyme elevations
Metabolic causes of vomiting
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
