between the elements of the emetic reflex.
Primary GI diseases are those where there is specific primary GI pathology such as gut disturbance due to dietary indiscretion, inflammation, infection, parasites, obstruction or neoplasia. There may be metabolic consequences of the GI disease, but the primary pathology is in the GI tract.
Secondary GI disease is where the vomiting or regurgitation has occurred due to pathology elsewhere in the body – the gut is just the ‘messenger’. Abnormalities of other body systems may indirectly cause vomiting either due to the action of toxins on the CRTZ, vomiting centre and vestibular system or by stimulation of peripheral non‐GI‐associated vomiting receptors.
Examples would include renal failure, liver disease, ketoacidososis, pancreatitis, hypercalcaemia, hypoadrenocorticism and other metabolic disorders. In most cases, there is no pathology identifiable in the gut, or where there is, for example, ulceration secondary to liver disease, uraemia or hypoadrenocorticism, the primary cause is the metabolic disorder. While symptomatic management strategies might be directed at the gut pathology in these cases (such as the use of anti‐ulcer drugs), there is no diagnostic benefit to imaging the gut, for example, by endoscopy.
Why is it important to differentiate primary from secondary GI disease?
It is important to determine whether primary or secondary GI disease is occurring in the vomiting or regurgitating animal, as much time and money can be wasted if the wrong system is investigated. As discussed in Chapter 2, the range of diagnoses to consider, diagnostic tools used and potential treatment or management options for primary, structural problems of a body system such as the GI tract are often very different compared to those relevant to secondary, functional problems of that system. Investigation of primary GI disease often involves some form of imaging modality (radiology, ultrasound, endoscopy and surgery) and/or biopsy. Routine haematology and biochemistry are often of little diagnostic value in GI disease, although they may give clues about the clinical status of the patient. In contrast, for secondary GI disorders, haematology, biochemistry and other tests are often critically important in progressing towards a diagnosis.
It is also important to appreciate that there are cases of primary GI disease causing vomiting, such as gastroenteritis caused by dietary indiscretion or other irritants, that can be safely treated symptomatically, as the cause is transient and will resolve within days without specific treatment. Symptomatic management such as withholding food, antiemetic treatment and/or dietary change is appropriate for these patients. However, there are few, if any, secondary GI causes of vomiting (such as liver disease, renal failure, hypoadrenocorticism and hypercalcaemia) where the cause is transient, which will respond to symptomatic treatment and/or will resolve without specific therapeutic intervention.
The uncommon secondary GI causes of regurgitation all cause megaesophagus (Table 3.2), so the clinical decision pathway leading to their diagnosis begins with the diagnosis of megaoesphagus by endoscopy or diagnostic imaging and then the search for a metabolic cause. As mentioned, symptomatic treatment of regurgitation without establishing the cause is not prudent.
Thus, the clinician’s clinical reasoning, in the consultation room, about whether primary or secondary GI disease is likely to be present is a crucial component of the rational management of patients reported to be vomiting or regurgitating and of clear communication with the client.
What are the clues that the patient has primary or secondary GI disease causing vomiting?
Primary GI disease should be strongly suspected if:
An abnormality is palpable in the gut, for example, foreign body and intussusception
The vomiting is associated with significant and concurrent diarrhoea
The patient is clinically and historically normal in all other respects
The onset of vomiting significantly preceded any development of signs of malaise – depression and/or anorexia
The vomiting is consistently related in time to eating (although this can also occur with pancreatitis).
It is important to note, however, that primary GI disease cannot be ruled out even if none of the aforementioned features are present. For example, vomiting may be delayed for some hours (up to 24 hours) in animals with non‐inflammatory gastric disorders. Animals with foreign bodies or secretory disorders of the bowel often vomit despite not eating. In lower bowel disorders, vomiting more commonly occurs at variable times after eating.
Animals with primary GI may also be depressed and inappetant due to the lesion (there are neural inputs to the satiety centre in the hypothalamus from the gut) or due to the secondary effects of prolonged vomiting with dehydration or electrolyte disturbances. Usually, the malaise will occur at the same time or after the onset of vomiting.
Thus, the features in the aforementioned bulleted list are strong clues that primary GI disease is present, but their absence does not preclude it.
Animals with secondary GI disease are vomiting due to the effect of toxins on the vomiting centre or CRTZ or because of the stimulation of non‐GI‐associated peripheral receptors. The vomiting is usually unrelated to eating – except pancreatitis in dogs.
With secondary GI disease:
Animals will often have evidence from the history and/or clinical examination of abnormalities affecting other organ systems, for example, jaundice, polyuria/polydipsia (PU/PD).
Vomiting is usually intermittent, unrelated to eating and may often occur subsequent to the onset of other signs of malaise.
In general, animals that are vomiting due to extra‐GI disease are metabolically ill and are not usually bright, alert and happy.
If a patient has been metabolically ill (depressed and inappetant) for a significant period before vomiting was observed, then secondary GI disease is more likely.
Secondary GI causes of regurgitation will frequently have other systemic signs such as generalised weakness or metabolic malaise. It is usually only patients with megaoesophagus due to focal myasthenia gravis who present with regurgitation as their only clinical sign.
Exceptions to the ‘rules’
The exception to these generalisations about the features of secondary GI disease is pancreatitis in dogs. Canine pancreatitis behaves similarly to a primary GI disease in that it causes acute‐onset vomiting in an initially often otherwise well dog and often subsequent to an episode of dietary indiscretion. The vomiting often occurs immediately after eating, and decreased appetite and depression may not precede the onset of vomiting.
Pancreatitis in cats, however, usually behaves similarly to a secondary GI disease. Cats with hyperthyroidism may also vomit intermittently over a prolonged period and seem otherwise well (although, of course, they may also have other clinical signs suggestive of hyperthyroidism).
If primary GI disease is determined to be present, the temporal relationship of vomiting to eating and the character of the vomitus should be used to assess where the lesion is likely to be – the upper or lower GI tract.
Diagnostic tools such as contrast radiography may be appropriate to localise the lesion. An assessment of the likely location of the lesion is important, as this may determine what further diagnostic procedures are suitable. For example, endoscopy would be appropriate for examining the stomach and possibly duodenum but will be of little use if lower small bowel disease is suspected.
Defining