A FEW WORDS... Acute Vomiting in Dogs and Cats (from Ep 9)

Vomiting in dogs and cats is one of the most common presentations we see in general practice. It can be straightforward and self-limiting, or it can be the first sign of something far more serious. One of the biggest challenges is that “vomiting” has numerous causes and sequelae that can be difficult to predict, so superb communication is paramount.

In this post, we’re taking a practical look at how to approach acute vomiting in dogs and cats in general practice: from distinguishing vomiting from regurgitation, to taking a useful history, recognising instability, deciding when empirical treatment is appropriate, and knowing when to investigate further.

Vomiting or regurgitation?

First things first: Is it vomiting or regurgitation?

Before diving into differentials, we must define the physical event. The distinction is critical because it dictates your entire diagnostic path.

Vomiting: The Active Reflex

Vomiting is a coordinated, active process mediated by the emetic center in the brain. It is almost always preceded by signs of nausea—lip-smacking, hypersalivation, and food aversion—followed by forceful abdominal contractions and retching. The expelled material originates from the stomach or proximal small intestine.

Regurgitation: The Passive Flow

By contrast, regurgitation is passive. There is no heaving, no abdominal effort, and often no warning. Food or fluid is brought back up—usually shortly after ingestion—and typically reflects esophageal disease rather than primary gastric pathology. Owners often don't realize it has happened until they find the puddle.

Why the distinction matters:

If you confirm true regurgitation, your differential list shifts dramatically toward esophageal disorders:

Motility issues: Megaesophagus secondary to Myasthenia Gravis or vascular ring anomalies.

Anatomical/Obstructive: Vascular ring anomalies, esophageal foreign bodies, or strictures.

The "Grey Zone": When the Lines Blur

Real-life clinical presentation isn't always tidy. Several scenarios can mimic regurgitation despite being gastric in origin:

Brachycephalics & Hiatal Hernias: These patients often experience "silent" reflux or "sicky burps"—a sudden, quiet expulsion of gastric contents with minimal retching.

Severe Gastroenteritis: In cases of extreme mucosal irritation, the threshold for the vomit reflex is so low that the stomach may expel contents with very little abdominal effort.

The "Overflow" Phenomenon (Obstruction): In patients with a distal GI obstruction, the stomach becomes a high-pressure reservoir of fluid. These animals (especially cats) may experience "passive" vomiting where liquid simply overflows the gastroesophageal sphincter.

Clinical Pearl: Be extremely cautious with obstructed patients during anesthetic induction. A stomach full of fluid under pressure can "regurgitate" instantly as the upper esophageal sphincter relaxes, leading to a high risk of aspiration pneumonia.

What does nausea look like?

Recognising nausea can be very helpful, especially in patients that are not actively vomiting in the consult room.

In dogs and cats, signs of nausea can include:

• lip-smacking

• hypersalivation

• repeated swallowing

• restlessness

• food interest followed by food aversion

• turning away from treats

• hunched posture

These signs can help support the interpretation that you are dealing with a vomiting/nausea syndrome rather than a pure regurgitation problem.

History taking: where the real diagnostic work begins

A good history often points you towards your most likely differentials before you even put hands on the patient.

Some of the most useful questions include:

Fluid losses and hydration risk

A rough sense of fluid in versus fluid out can be surprisingly valuable. If a pet has had repeated vomiting, watery diarrhoea, and poor intake for 24 hours, dehydration becomes much more likely. Owners are rarely able to quantify this accurately, but the conversation itself is still useful.

Diet history

Ask about recent diet changes, new treats, table scraps, scavenging, bin raiding, beach finds, or access to non-food items. Owners do not always volunteer these details unless prompted in a very practical way — for example, “Have you noticed anything missing?” or “Have you seen them pick anything up on walks recently?”

Foreign body risk:

This should always be tailored to the animal in front of you. A young, ball-obsessed Boxer is a very different foreign body candidate from an elderly arthritic Labrador who barely leaves the house.

Stool quality:

It is worth asking specifically about faeces, because “soft stools” can mean very different things to different owners. Asking whether stools are “pick-up-able” is often far more useful than asking whether they have diarrhoea.

Blood in vomit or faeces:

Owners are often highly alert to blood and may volunteer this before you ask, but it still needs characterising. A few streaks of fresh blood in a bright dog with gastritis is very different from persistent haematemesis in a dull patient.

Medication history:

This is a huge one. Ask not just what the pet has been prescribed, but what the owner may have given at home, what the other pets in the house are on, and what human medications might have been accessible. NSAIDs are especially important, but so are accidental ingestions of other drugs.

Signalment and age:

Age changes your differential list substantially. Young animals are more likely to have dietary indiscretion, parasites, parvovirus, foreign bodies or toxin exposure. Older patients push you more towards metabolic disease, organ dysfunction and neoplasia.

Acute flare up of chronic problem:

I'm looking if a longer term gut issue has flared up. Do make sure you ask if this is a ‘sicky patient’ usually? Do certain foods upset their tummy? Are upset tummies frequent? In dogs, can stools can be picked up without leaving anything behind? In cats, I ask, if they see the stools, are they solid sausages (a few owners will notice them in the garden now and then)? Furthermore, in cats, do they have frequent furballs? Or grassy vomits? Or, what I call, piggy or greedy vomits? This is where they gobble the food up and bring it up mostly unchanged soon after. Check the notes for previous gastroenteritis episodes.

Examination: stabilise before you investigate

When faced with a vomiting patient, particularly one that looks unwell, the first question is not “what is causing this?” It is “is this patient in shock?”

For any sick, vomiting patient, it is worth returning to basic emergency priorities.

Cardiovascular assessment:

Look at mucous membranes, CRT, pulse quality and heart rate. Dogs with significant hypovolaemia often show tachycardia, weak pulses, pale mucous membranes and prolonged CRT. Cats can be trickier and may present with bradycardia and hypothermia instead.

Respiratory assessment:

Check respiratory rate, effort and chest sounds. This is particularly important in brachycephalic dogs and in any patient where aspiration is a concern.

Neurological/mentation assessment:

Is the patient bright, quiet, depressed, collapsed, ataxic? A collapsed vomiting patient is an entirely different prospect from the bouncy dog that vomited twice this morning and is now trying to eat the bin.

Hydration versus shock:

This is a distinction worth making clearly.

Dehydration reflects total body water loss. You may see tacky mucous membranes and skin tenting. If you have a recent weight, you can look for weight loss. 5% dehydrated represents 1kg weight loss in a 20kg dog, or 0.25kg in a 5kg cat.

Hypovolaemic shock reflects inadequate circulating blood volume. You may see tachycardia, poor pulses, pale mucous membranes, prolonged CRT, weakness and collapse.

The treatments are not the same. Shock needs urgent IV fluid resuscitation, the so-called shock boluses. Dehydration correction is slower and more calculated. Of course, both can exist at the same time.

Initial stabilisation priorities:

If the patient is in hypovolemic shock, treatment should be commenced immediately. Typical examination findings would be a fast heart rate, pale mucous membranes, weak pulses and reduced capillary refill time. The history may suggest rapid fluid loss from vomiting or diarrhoea and a lack of drinking. Sometimes the fluid is hiding within the bowel or stomach lumen and has not been expelled….. yet!

1. IV access and fluid therapy:

Balanced crystalloids (e.g. Hartmann’s/LRS) are appropriate for most patients.

However, in patients with suspected hypochloraemic metabolic alkalosis (e.g. pyloric obstruction), 0.9% NaCl may be preferred due to its higher chloride content.

Initial resuscitation boluses:

Dogs: 10–20 ml/kg over 10–15 min

Cats: 5–10 ml/kg over 10–15 min

Reassess after each bolus (HR, perfusion, lactate, BP) and repeat as needed.

2. Take samples when you place the catheter

Every catheter placement is a sampling opportunity. Even if you are not yet certain what you want to test, get blood before fluids if you can. Minimum database options such as PCV, TS, glucose, lactate and basic biochemistry can be incredibly helpful.

3. Oxygen where appropriate

Collapsed, flat or severely compromised patients should receive oxygen support where possible.

4. Analgesia

Pain and nausea are often underappreciated contributors to distress, tachycardia and poor recovery. Opioids can be very useful, but dose thoughtfully and be aware of dysphoria, sedation, nausea and reduced GI motility. Clinical judgement matters here.

Empirical treatment or full work-up?

This is where real-world general practice decisions come in.

Not every vomiting patient needs an immediate full diagnostic work-up. A lot of patients are bright, well hydrated, comfortable, and have very little of concern on history or clinical exam. In these animals, symptomatic treatment with clear return instructions is often appropriate.

A reasonable framework might look like this:

Likely suitable for symptomatic treatment

• acute vomiting

• bright and alert

• normal vitals

• eating or still interested in food

• no weight loss

• no concerning abdominal pain

• no major red flags in the history

More likely to need bloods and/or imaging

• lethargy or reduced mentation

• prolonged anorexia

• dehydration

• abdominal pain

• repeated or protracted vomiting

• suspected foreign body

• rectal temperature 36C or 37C

• abnormal clinical exam

• significant haematemesis or melaena

Often the discussion with the owner centres around three tiers for the non-shocky patient. This tiered approach is often helpful both clinically and financially.

1. symptomatic treatment and monitoring

Anti-emetics, typically maropitant or ondansetron.

Metoclopramide is suggested by some veterinarians, and can be especially considered for ileus, improved gastric emptying.

Consider subcutaneous fluid in dehydrated patients if the client cannot afford or declines hospitalisation. I will try to give them a minimum of 20ml/kg subcutaneously in this situation. And warn them first that there will be a fluid bubble where the fluid has been injected for several hours. I tell them they will look like a camel afterwards! I find it administered best using a big pink hypodermic needle at the end of a giving set attached to the fluid bag. I find my patients don't particularly notice the insertion of a big pink needle for some strange reason. Just squeeze the fluid bag to get the fluid into the subcutaneous space as quick as possible. Use more than one site if you wish.

Tempt, as nutrition is vital to feed the enteral cells. Little and often. Ideally something simple like chicken or low fat.

Encourage them to drink, but don't allow them to drink too much at once, or they may vomit it back up. Proprietary dehydration liquid is used by some. I prefer trying the cooking fluid if home-cooking chicken in water for example.

2. Initially blood work then chat again after results

For some clients, I will just suggest an in-house blood test to gather more evidence. When the results come in thirty minutes, I tell them we can put all the evidence together from the history, examination and blood test results to make a plan. This gives them time to think about the logistics and the decision. This can help compliance for some clients, especially when the decision to admit comes as a surprise.

3. Admit blood work plus imaging

For concerned clients, I will simply admit for blood testing and imaging. Depending on cost, I may get started with some fluids. With anything shocky (tachycardia, pale or extended CRT), that means a bolus or two.

For non-shocky patients that may not need dedicated out-of-hours care (and associated cost), I will concentrate into trying to get at least half their estimated fluid loss (dehydration) resolved in the remaining time to collection. Clearly if it's 4pm, this may not be feasible. Because most of my practices will ask for collection at 6pm, if I admit a patient at 11am, I'll have 7 hours of fluids. If I suspect they are 5% dehydrated from history and examination, I'll aim to get at least 2.5% (25ml per kg of body weight) of their body weight into them via ivft over the time available, potentially adding more for ongoing losses (profuse vomiting or watery diarrhoea) as they occur. I may use subcutaneous fluid to aid hydration if costs are an issue, especially near time of discharge to continue parenteral fluid administration beyond collection time. It's important to be mindful of overloading patients with too much fluid too quickly. And I am always very cautious with patients with a heart murmur.

A note on antiemetics: useful, but not a substitute for thinking

Maropitant is widely used and often very effective at improving comfort in vomiting patients. In many acute, otherwise uncomplicated cases, it is a reasonable empirical option.

The important caveat is that antiemetics should not give false reassurance. If a patient continues to vomit despite antiemetic cover, or worsens over the next 12–48 hours, that should prompt re-evaluation and often further work-up.

There are also cases where “maropitant failure” is not treatment failure at all — it is misclassification. If the patient is regurgitating rather than vomiting, maropitant may not solve the real problem.

Other antiemetics and prokinetics may have a role in selected cases, but the bigger clinical lesson is not which drug is “best” in every scenario. It is remembering to ask whether the diagnosis still makes sense if the patient is not improving.

What about omeprazole?

Many of us were trained in an era where vomiting or diarrhoea in a hospitalised animal often meant automatic acid suppression. That approach is now worth questioning.

Omeprazole and other acid suppressants probably make most sense when there is genuine concern about:

• reflux or oesophagitis

• severe GI bleeding

• gastric ulceration

• NSAID-associated gastric injury

Used thoughtfully, they absolutely have a place. Used reflexively in every vomiting patient, probably less so.

Common differentials for vomiting

Vomiting is not a diagnosis — it is a symptom. Causes range from self-limiting gastritis to surgical emergencies to endocrine disease.

A practical way to think about differentials is by category.

Primary gastrointestinal causes

• acute gastritis/gastroenteritis

• dietary indiscretion

• food-responsive enteropathy/allergy

• parasites

• GI foreign body

• intussusception

• oesophageal foreign body

• GI ulceration

• ileus

• GI neoplasia

Extra-GI causes

• pancreatitis

• chronic kidney disease

• hepatic disease

• Addison’s disease

• diabetes mellitus / DKA

• pyometra

• prostatitis

• peritonitis

• toxin ingestion

• neurological disease, including vestibular disease

Age helps prioritise the list, but it should never be used as a substitute for thinking. Old dogs can still eat bizarre things, and young animals can still be very sick.

Diagnostic work-up: what are we actually looking for?

Blood work:

A minimum database can go a long way. Useful early parameters include:

• PCV/TS for hydration status

• glucose for hypoglycaemia (especially pediatrics or wildlife) or diabetes

• lactate for perfusion concerns

• Blood gases and electrolytes can also help support certain suspicions. For example, a patient with vomiting, hypochloraemia, hypokalaemia and metabolic alkalosis may push a proximal GI obstruction higher up the list, or high k+ in typical Addison's.

• haematology and biochemistry for inflammation, organ dysfunction and metabolic disease

• T4 in older cats

• snap tests where appropriate, such as parvo, cPLI or fPLI

• Bilirubin can be helpful, and in cats especially can often occur with pancreatitis due to extra-hepatic obstruction of the bile duct.

  
  

Imaging

For many vomiting patients, abdominal ultrasound is an excellent first imaging choice. It is non-invasive, usually well tolerated, and can quickly answer useful questions:

• is there free fluid?

• Are there two populations of bowel?

• Typically (proximal to the obstruction) bowel loops distended with copious fluid and (distal to the obstruction) normal bowel loops?

• is the stomach very dilated with fluid?

• is there normal or even hyperkinetic peristalsis or ileus?

• Sometimes large volumes of fluid can be seen in the colon, which would indicate more fluid loss from diarrhoea imminently

• is the pancreas enlarged or inflamed?

• is the uterus enlarged with fluid?

• are there masses or organ abnormalities?

Abdominal radiographs are often complimentary to ultrasound, rather than an alternative. They have an important role too, especially for radiopaque foreign bodies (stones, peach stone, metal, balls, toys), megaoesophagus or oesophageal obstruction, or identifying gas build up in obstruction or constipation/obstipation, or even masses.

Exploratory laparotomy as both a diagnostic and therapeutic tool

An exploratory laparotomy is sometimes both a treatment and a diagnostic tool. A negative ex lap is not a failure if it was clinically justified and clearly discussed with the owner in advance.

When I’m considering surgery, I talk the owner through the evidence for a possible obstruction and explain the uncertainty. I make it clear that we’ve discussed the case as a team where possible, and outline the options available.

A key part of the conversation is balancing risk — the risk of surgery versus the risk of missing an obstruction that may deteriorate and become life-threatening. In some cases, I feel it is safer to proceed with surgery than to delay and potentially miss something significant.

That said, I also emphasise that we will gather as much evidence as possible beforehand — imaging, bloods, clinical progression — and that surgery is not a first step, but a justified decision when uncertainty remains and risk is high.

Cats: the chronic vomiters we normalise too easily

Cats deserve their own section because owners — and sometimes vets — can underestimate chronic GI signs in them.

Hairballs are the classic example. While occasional hairball production may be brushed off as “normal,” frequent hairballs should raise suspicion. Weekly hairballs are not something to ignore. Even every two to four weeks, particularly if long-term, should prompt thought about chronic enteropathy. Mild cases are often much improved with diet changes alone. My initial diet plan is poultry or rabbit based. Avoiding beef, fish, seafood and dairy especially.

Other feline signs that often get normalised include:

• eating grass and vomiting (grassy vomits)

• “scarf and barf” episodes (piggy vomits)

• intermittent appetite fluctuation

• recurrent “sensitive stomach”

• chronic low-grade vomiting

• Two or three episodes of diarrhoea annually in my mind indicate a likely enteropathy, typically dietary in aetiology.

  
  

Brachycephalic dogs: why “sicky burps” matter

Brachycephalic dogs, especially French Bulldogs, commonly blur the line between vomiting and regurgitation.

Because of upper airway obstruction, these dogs generate marked negative intrathoracic pressures. Over time, that may contribute to hiatal laxity, reflux and oesophageal dysfunction. The result can be those classic quiet, effortless episodes of reflux or regurgitation that owners may barely notice until they step in them.

This matters in practice because treatment may need to address more than nausea alone. Depending on the case, the plan may involve a combination of:

• antiemetics

• acid suppression

• prokinetics

• management of airway disease

• investigation for hiatal or reflux-related pathology

Practical take-home points

Vomiting cases can feel deceptively simple, but a structured approach makes a huge difference. The key practical points are:

• Make sure you are dealing with vomiting and not regurgitation

  
  

• Stabilise shocky patients before chasing the diagnosis

  
  

• Use history to guide your differentials

  
  

• Distinguish dehydration from shock

  
  

• Be selective, but thoughtful, about empirical treatment

  
  

• Reassess quickly if the case is not improving

  
  

• Remember that vomiting is often a sign of disease outside the GI tract

  
  

• In cats and brachycephalics especially, don’t dismiss chronic or subtle signs too easily

Final thoughts

Acute vomiting in dogs and cats is one of those bread-and-butter presentations that can be either completely routine or unexpectedly serious. The trick is not to overcomplicate every mild case, but equally not to miss the unstable, atypical or non-responsive ones.

A calm, methodical approach goes a long way: take a thorough history, assess stability, perform a focused examination, prioritise diagnostics sensibly, and provide clear safety-netting.

Keep the client informed throughout and actively check in on how they feel about each proposed step. This not only builds trust, but helps you tailor your investigation and treatment plan to their individual circumstances. Remember, clients are often juggling other responsibilities — caring for family members, managing work, or doing the school run — and good veterinary care should take their realities into account as well.

References and papers mentioned

Norsworthy GD et al. (2013). Diagnosis of chronic small bowel disease in cats: 100 cases. JAVMA 243(10):1455–1461.

Cannon M. (2013). Hair balls in cats: a normal nuisance or a sign that something is wrong? J Feline Med Surg 15

Zoran DL. (2002). The carnivore connection to nutrition in cats. J Am Vet Med Assoc. 221(11):1559–1567.

Henze L et al. (2022). Ondansetron in dogs with nausea associated with vestibular disease. J Vet Intern Med. 36(5):1726–1732.

Conte A et al. (2020). Computed tomographic comparison of esophageal hiatal size in brachycephalic and non-brachycephalic breed dogs. Vet Surg. 49(8):1509–1516.

Eivers C et al. (2019). Retrospective analysis of esophageal imaging features in brachycephalic versus non-brachycephalic dogs. J Vet Intern Med. 33(4):1740–1746.

Burke JE et al. (2021). Effectiveness of orally administered maropitant and ondansetron in preventing preoperative emesis and nausea in healthy dogs. J Am Vet Med Assoc. 260(S1):S40–S45.

Kraus BLH. (2014). Efficacy of orally administered maropitant citrate in preventing vomiting associated with hydromorphone administration in dogs. JAVMA 244(10):1164–1169.