Emesis in dogs: a review

Abstract

Emesis is a common presenting sign in small animal practice. It requires a rational approach to management that is based upon a sound understanding of pathophysiology combined with logical decision making. This review, which assesses the weight of available evidence, outlines the physiology of the vomiting reflex, causes of emesis, the consequences of emesis and the approach to clinical management of the vomiting dog. The applicability of diagnostic testing modalities and the merit of traditional approaches to management, such as dietary changes, are discussed. The role and usefulness of both traditional and novel anti-emetic drugs is examined, including in specific circumstances such as following cytotoxic drug treatment. The review also examines areas in which common clinical practice is not necessarily supported by objective evidence and, as such, highlights questions worthy of further clinical research.

Figure 1

A diagrammatic representation of the series of events comprising the emetic reflex in the dog. LES: Lower oesophageal sphincter. UES: Upper oesophageal sphincter. Summarised from: ( Abe and others 1993 [2b], Abe and others 1994 [2b], Furukawa and Okada 1994 [2b], Koga and others 1998 [2b], Koga and Fukuda 1990 [2b], Lang and others 1986b [2b], Lang and others 1986a [2b], Lang and others 1993 [2b], Lang and others 2002 [2b], Onishi and others 2007 [2b], Sha and others 1996 [2b]). [OEG C.]

Figure 2

An algorithm to guide the approach to the management of emesis in the dog. If the patient is initially treated symptomatically, re‐examinations should be scheduled and the patient re‐assessed for criteria of concern (see table 8) that might prompt further investigation. [OEG D]

Figure 3

Schematic diagram of the vomiting reflex indicating probable sites of action of antiemetic drugs. Peripheral emetogens (e.g. ipecac) stimulate the pharynx or stomach where Neurokinin‐1 receptors are involved in local sensory nerve activation and 5‐HT3 receptors are involved in modulating the activity of visceral afferent nerves which convey the sensory information to the CNS. Stimuli which cause vomiting can also reach the CNS through the blood stream (e.g. toxins – central emetogens; e.g. apomorphine) to stimulate the chemoreceptor trigger zone. Within the central nervous system, inputs are integrated and the relayed to the ‘vomiting centre’ a collection of neurones in the brain stem which are thought to be the origin of the efferent arm of the vomiting reflex. Vomiting is elicited when the integrated inputs exceed the threshold and the motor output from these neurones leads to the co‐ordinated action of vomiting