SA V+
Approach to vomiting
History | · How long been going on for? – acute vs chronic · Are they a scavenger? Access to any toxins? · Any recent diet changes? · Any other animals in house affected? – if yes = infectious causes · Nature of vomit – amount, colour, frequency? · Any diarrhoea? – suggests intestinal cause · Previous abdominal surgery? History of oesophagitis? · Vaccination and worming status? · Any gagging/retching/coughing? – want to differentiate from regurgitation |
Clinical examination | · Hydration status · BCS – differentiate acute vs chronic (BCS loss) · MM colour – anaemic? Jaundiced? · Check under tongue – linear FB? · Abdominal palpation – any pain, thickening, effusion, palpable FB, organomegaly · Abdominal auscultation – ileus, borborygmi · Rectal examination – mass, FB, temperature · Neurological exam – is vomiting/vestibular system affected? · Any signs of systemic disease, e.g. pyrexia, PUPD, jaundice |
Further investigations | · Want to rule out obstruction – risk of acute death/sepsis (GIT can burst due to increased pressure, necrosis due to decreased blood supply) · Blood sample o Haematology – assess hydration status, infectious diseases o Biochemistry – look at liver/renal parameters, investigate metabolic disease · Abdominal radiography – FB, masses, distended SI · Abdominal U/S – loss of serosa, free fluid, intestinal wall thickness, neoplasia, intussusception · Specific tests once more localised cause o Faecal analysis o FeLV/FIV snap test o Total T4, ACTH, cPLI |
Management | · Don’t want to give anti-emetics straight away as vomiting may be beneficial o But if >12h AND RULED OUT FB – give anti-emetic (will feel better, encourage eating) § Maropitant – good for metabolic, CRTZ, vestibular § Metoclopramide – also prokinetic, if FB could rupture GIT · Supportive – GI diet (feeding tube if still not eating), gastroprotectant (omeprazole), prokinetics if D+, IVFT to replace ongoing losses · Treat underlying cause, e.g. treat metabolic disease, surgical removal of obstruction |
Regurgitation | · Passive expulsion of food – undigested, soon after eating · Treatment: o Maintain hydration/replace losses with IVFT o Trial different food types o Treat underlying cause: § Megaoesophagus – no treatment, just feed small amounts from height § Oesophagitis – PEG tube to bypass § Oesophageal FB – surgical removal |
Causes of vomiting
Acute vomiting | · GI tract o Obstructive – FB, neoplasia, parasitic, constipation, intussusception/volvulus o Inflammatory – gastritis, gastroenteritis, colitis o Mucosal insult – dietary indiscretion/intolerance, sudden diet change, toxins o Infectious – viral, bacterial, parasitic o Gastric stretch · Cerebral cortex – increased ICP, head trauma · Vestibular system – motion sickness, idiopathic vestibular disease, otitis interna · CRTZ o Endogenous – DKA, Addison’s, AKI, pancreatitis, pyometra, hepatitis, peritonitis o Exogenous – toxins, drugs (e.g. NSAIDs causing ulcers) |
Chronic vomiting | · GI tract o Chronic inflammatory – gastritis, gastroenteritis, colitis, chronic enteropathy o Mucosal insult – dietary intolerance o Infectious – viral, bacterial, parasitic o Obstructive – pyloric FB, neoplasia, parasitic, constipation · Cerebral cortex – neoplasia/SOL, CNS disease · Vestibular system – chronic vestibular damage, otitis interna, neoplasia, cerebellar disease · CRTZ o Endogenous – diabetes mellitus, Addison’s, chronic renal failure, liver failure, chronic pancreatitis, hyperthyroidism (cats) |
Regurgitation | · Dilation – megaoesophagus · Obstruction o Intraluminal – FB, stricture (secondary to oesophagitis, post GA) o Mural – neoplasia, inflammation o Extramural – vascular ring anomaly, hiatal hernial, neoplasia/SOL · NM disorders – myasthenia gravis, botulism, tetanus, distemper, Addison’s, hypothyroidism |
Dysphagia | · Pain on closing mouth (dental disease, stomatitis), opening mouth (retrobulbar abscess) or both (jaw fracture, TMJ disease) · Failure of NM control – CN disease, CNS disease, masticatory myositis, botulism, myasthenia gravis · Obstruction, e.g. pharyngeal FB, poly, neoplasia, abscess, lymphadenopathy |
GI neoplasia’s | · Most common: o Adenocarcinoma (most common in dogs) § If gastric – see haematemesis (coffee granules) § If SI/colonic – see ribbon-like faeces o Leimyosarcoma o Lymphoma (most common in cats) o Polyps · Diagnosis: full thickness biopsy, mets check · Treatment: surgical excision +/- draining LNs |
Approach to diarrhoea
History | · How long been going on for? · Up to date with vaccinations and worming protocols? Any medications? · Are they a scavenger? Access to toxins? What diet are they on? Any recent changes? · Nature of diarrhoea? Appearance? Frequency? – yellow + fatty = EPI, blood = LI, incr. frequency = LI, increased volume = SI · Are they straining? – tenesmus = LI · Any vomiting? Are they still eating · Any other clinical signs? – pruritus = food responsive enteropathy · Any other animals in house affected? · Previous abdominal surgery? · Want to differentiate between SI and LI o SI = weight loss, watery/bulky faeces, increased volume, 1-3x daily, no tenesmus, no mucus, no melena o LI = no weight loss, appearance varies, normal/decreased volume, >6x a day, tenesmus, mucus, fresh blood present · Age of animal? – young puppy or old unvaccinated dog = parvo |
Clinical examination | · Hydration status · BCS/weight loss? – differentiate acute vs chronic, weight loss = chronic SI · Abdominal palpation – any pain/discomfort? Thickened intestines, palpable FB · Abdominal auscultation – ileus, borborygmi · Rectal examination – temperature, mass, FB, blood · Cardiac abnormalities – addisons, cardiac disease · Signs of systemic disease, e.g. pyrexia · Palpable thyroid · Examine skin – poor coat = food sensitivity |
Further investigations | · Blood sample for haematology o Anaemia – chronic disease, GI bleeding o PCV – increased = dehydration o Inflammatory leukogram – inflammation, infection, parasites o Lymphopenia – lymphangiectasia o Eosinophilia – parasites, hypoadrenocorticism o Lymphocytosis – neoplasia, hypoadrenocorticism · Blood sample for biochemistry – looking for markers of systemic disease o Total proteins – increased = dehydration o Albumin + globulin – decreased = PLE, high globulin = FIP o Azotaemia (high urea + creatinine) – dehydration § High urea + low protein – GI bleeding § Low urea + low cholesterol, albumin + glucose = functional liver disease o Electrolytes – abnormalities = fluid imbalance, high K + low Na = hypoadrenocorticism o Liver enzymes – increased ALT = EPI o Cholesterol – low cholesterol = malabsorption, functional liver disease · TLI if suspect EPI – will be decreased · Urinalysis – USG – marker of hydration status and renal disease · Faecal analysis o Culture – campylobacter, salmonella, E. coli o Faecal parasitology – giardia o Faecal virus tests – SNAP test = parvo, PCR = campylobacter, parvo · Imaging – U/S, radiography, endoscopy – thickened intestinal wall = steroid responsive enteropathy, look for tumour |
Management | · General symptomatic treatment: o IVFT to restore losses, tx dehydration – Hartmann’s (has buffering capacity) o Bulking agents: peridale 98% - increases bulk of intestinal contents, promotes peristalsis o Prebiotic: lactulose, probiotics o Prokinetics: metoclopramide – for chronic D+, reduces ileus, promotes motility o Antibiotics – if evidence of sepsis, or based on C+S · Parvovirus – aggressive IVFT, amoxicillin, maropitant, metoclopramide · Campylobacter – fluroquinolones · Food responsive enteropathy – diet trial to rule out, should see GI improvements in 1w · Steroid responsive enteropathy – dietary support |