CHAPTER 3 Vomiting, regurgitation and reflux
Jill E. Maddison
Department of Clinical Science and Services, The Royal Veterinary College, London, UK
The why
Veterinarians in general practice frequently assess animals whose owners report they are vomiting.
The causes and consequences of vomiting can range from clinically inconsequential to life threatening.
In contrast, regurgitation is a much less common clinical sign. Almost invariably, the patient who is truly regurgitating as their primary clinical problem will have serious disease.
Gastric reflux can also be confused with vomiting and has different implications for the animal that need to be recognised.
It is therefore essential that the clinician has a robust and rapid way to assess patients during the initial consultation so that rational decisions can be made about appropriate diagnostic and/or therapeutic plans.
Pathophysiology
The main function of vomiting is to protect the animal from ingested toxins. Dogs in particular have a propensity to eating disgusting things and have a very well‐developed vomiting reflex.
To develop a rational approach to the patient who is reported to be vomiting, it is important to appreciate the pathophysiology of vomiting and regurgitation.
Vomiting or emesis is the forceful expulsion of gastric contents through the oesophagus, mouth and, sometimes, nostrils. It is a neurologically complex process resulting from the synchronised activity of a number of abdominal, pharyngeal and thoracic structures. The act of vomiting is coordinated in the medulla oblongata and cannot occur without a functional vomiting centre. In contrast, regurgitation is a passive process, which involves the retrograde movement of food and fluid from the oesophagus, pharynx and oral cavity without the initiation of reflex neural pathways other than the gag reflex.
The essential neurological components of the emetic reflex are the following:
Visceral receptors
Vagal and sympathetic afferent neurons
Chemoreceptor trigger zone (CRTZ)
Vomiting centre within the reticular formation of the medulla oblongata.
It is important to understand the stages that occur in the act of vomition, as they contribute to the clinical manifestation of vomiting, and this also assists the clinician to differentiate vomiting from regurgitation.
The first stage of vomiting is nausea. In this stage, gastric tone is reduced, duodenal and proximal jejunal tone is increased and duodenal contents reflux into the stomach. The patient often appears depressed, hypersalivates and as a result may exhibit repeated swallowing and/or lip‐licking behaviour.
As an aside, while most patients who vomit will also be nauseous, it is important to recognise that the neural pathways involved in nausea and vomiting are not the same. Indeed, the neural pathways involved in nausea are still not well understood. The clinical relevance of this is that drugs that are effective anti‐emetics may not be effective at reducing nausea. If signs of nausea and food aversion persist once vomiting is controlled, consider adding a drug that has good efficacy against nausea such as ondansetron to the patent’s management. Noting, of course, that the persistence of nausea may also reflect progress of the underlying disease.
The nauseous stage is followed by retching (an unproductive effort to vomit, also known as ‘dry heaves’) and then vomiting. When the animal vomits, the epiglottis is closed and the soft palate presses up against the nasopharynx. The abdominal muscles and the diaphragm contract. The contraction of the abdominal muscles is usually visible to an observant owner. The cardia then opens, the pyloric stomach contracts and vomiting occurs. Reverse peristalsis, cardiac rhythm disturbances and increased colonic motility may also occur during the vomiting process.
The closure of the epiglottis and pressing of the soft palate up against the nasopharynx protect against aspiration of gastric contents. In contrast, during regurgitation, which is a passive process without neurological coordination, these actions do not occur. As a result, aspiration pneumonia is a common sequela to disorders that cause regurgitation and less likely in vomiting unless the animal is obtund.
Initiation and the process of vomiting
Vomiting is essentially initiated by either humoral or neural pathways. The humoral pathway involves stimulation of the CRTZ within the medulla oblongata by blood‐borne substances. The neural pathway is through activation of the vomiting centre.
Vomiting centre
All animal species that vomit have a brainstem ‘vomiting centre’, which is a group of several nuclei that act in concert to coordinate the somatomotor events involved in expelling gastric contents. Non‐vomiting species such as horses, rodents and rabbits also have the brainstem nuclei and motor systems necessary for emesis but lack the complex synaptic interaction between the nuclei and viscera required for a coordinated reflex.
There does not appear to be a discrete vomiting centre within the reticular formation of the medulla oblongata. Rather, there is an ‘emetic complex’ that refers to groups of loosely organised neurons distributed throughout the medulla, which are sequentially activated and play a role in emesis. This complex will be referred to in this chapter as the vomiting centre, however, as conceptually this assists the understanding of the physiology and pathophysiology involved.
The vomiting centre receives input from vagal and sympathetic neurons, the CRTZ, the vestibular apparatus and the cerebral cortex. It may also be stimulated directly by blood‐borne toxins that can cross the blood–brain barrier (BBB).
Central stimulation
Central stimulation of the vomiting centre occurs via higher centres in the central nervous system (CNS). Stimuli include nervousness, unpleasant odours, pain and psychogenic factors. Opioids and benzodiazepine receptors have been implicated in centrally initiated vomiting, but their exact mode of action has not been well characterised pharmacologically. Centrally induced vomiting may also occur due to direct stimulation of the emetic centre by elevated cerebrospinal fluid pressure or CNS inflammation or neoplasia.
Vestibular apparatus
Labyrinthine dysfunction associated with motion sickness and middle/inner ear infection also has input into the vomiting centre via neural pathways arising from the vestibular system. The CRTZ is involved in this pathway in the dog but not the cat.
Chemoreceptor trigger zone
The CRTZ is located in the area postrema in the floor of the 4th ventricle. It has no BBB, therefore allowing toxins and chemicals that would normally be excluded from the CNS access to the brain. The CRTZ is stimulated by endogenous toxic substances produced in acute infectious diseases or metabolic disorders such as uraemia or diabetic ketoacidosis as well as by drugs and exogenous toxins.
