Vomiting - gastro-enteric disease Flashcards
- History
◦ Always ask about scavenging/foreign bodies/diet e.g. bones.
◦ Diarrhoea in puppies/kittens
‣ Intussusception is more likely
‣ Or worms – check worming status, or pre-emptively worm them if concerned.
◦ BCS – condition loss is a concern for more chronic disease
◦ Faecal output – if normal then obstruction is less likely.
◦ Other signs of disease e.g. PUPD - Clinical signs
◦ Abdominal palpation – pain or can you feel a swelling of the GIT?
‣ Faeces in the colon can trick you in cats – i.e. it’s constipated e.g. dehydration in renal failure.
◦ Signs of sepsis/hypovolaemia
◦ Mentation – dullness/lethargy/obtunded/stuporous – treat them all as serious - Point of Care Ultrasound (POCUS)
◦ Free fluid in the abdomen is always abnormal
◦ Perforating foreign body
◦ May be able to directly image what you can feel – e.g. intussusception - If you are concerned – advise haematology/biochemistry/electrolytes and further imaging – e.g. further ultrasound or radiography.
- Ultimately it is the owner’s decision – in my experience it’s better to be cautious rather than blasé
How would you approach treatment for non-obstructive vomiting?
Acute
* Symptomatic treatment is acceptable
* Most episodes of gastritis, gastroenteritis, dietary indiscretion, intolerance are self-limiting.
* Dietary modification/support – Gastrointestinal Diet.
* High bioavailability of protein
* Easily digestible Carbohydrate and fat
* Low fibre (both slow gastric emptying)
* Gastro-protectants and anti-emetics
How would you manage a ‘non-obstructive’ case that’s not getting better?
Acute, none-responsive to symptomatic treatment:
You might be wrong!! Consider obstructive again – re-evaluate.
Are other clinical signs developing:
- Diarrhoea/changes in faecal output
- Consider faecal samples for bacterial, viral, parasitic disease
- PUPD/changes in urination/drinking
- Biochemistry to assess for renal or hepatic disease e.g. Acute Kidney Injury
- Neurological signs
- Cranial nerve deficits/changes in vision -> cerebral disease
- Ataxia/head tilt -> vestibular system (check the ears)
- Pyrexia
- Look for the infectious/inflammatory focus -> POCUS, haematology, biochemistry
Specific Tests:
* T4 for hyperT4 in cats
* cPLI and fPLI – pancreatitis
* Electrolytes and acid/base – may be developing hypochloremic alkalosis – will need IVFT support
* Basal Cortisol - Addisons
What neoplasia is most common in dogs GI tract? What are its specific clinical signs? How is it diagnosed? Treament?
Adenocarcinoma is the most common tumour of the stomach and large intestine, found in small intestine also. Locally invasive and progressive neoplasm, reducing the luminal diameter. Therefore, additional clinical signs include:
* Gastric – haematemesis (“coffee granules”)
* SI and Colonic – ribbon like faeces
Diagnosis requires biopsy
* Full thickness is the most reliable.
* Endoscopic biopsies are superficial and may miss lesions.
* Ultrasound is not as sensitive as endoscopy at identifying abnormal tissue for FNA/biopsy
* Surgical biopsy is the most sensitive.
* Always do a met check (3 view CXR or CT), although intestinal neoplasms less commonly spread to the lungs.
Treatment – surgical excision +/- draining lymph nodes.
Prognosis – Gastric (6 months), SI (4 – 18 months), Colorectal (2-4 years)
What is the most common neoplasia of the GI tract in cats? How is it treated? What is the prognosis? How is it diagnosed?
Lymphoma – the most common GI neoplasm in cats.
As with dogs, diffuse, meaning chemotherapy is the main treatment.
Prognosis:
* Poorly differentiated, high-grade lymphoma – <3 months
* Well differentiated, low grade, small cell – 2 to 3 years
Overall thickness of small intestine wall is greater on ultrasound - diagnosis is very difficult
What are common causes of gastroduodenal ulceration? How is it diagnosed? Treatment? Prognosis?
Dogs>Cats
Common causes:
Steroids and NSAIDs, Neoplasia, Hepatic disease
Diagnosis – endoscopy. Ultrasound is less sensitive, but will detect free fluid/gas if perforation has occurred.
Treatment – evidence is poor for all of these.
H2 receptor antagonist (e.g. Cimetidine) OR Proton pump inhibitor (e.g. omeprazole)
Sucralfate
Misoprostol – primarily consider in NSAID toxicity
Prognosis – completely depends on the underlying disease process.
How can you treat lymphocytic-plasmacytic gastritis and eosinophilic gastritis?
They both represent and abnormal, over-reaction of the local immune system. Dietary allergens (usually proteins) or antigens are probably the cause.
* Therefore, treatment is either remove the allergen/antigen or suppress the immune response (or both)
- Diet trial with hypoallergenic diet:
◦ Hydrolysed protein (commercially available, easy)
◦ Novel protein source (harder to source, probably more palatable) - Immunosuppression
◦ Prednisolone
◦ +/- azathioprine
◦ +/- cyclosporin
◦ +/- chlorambucil