Overview
Drugs used in the management of esophageal disease
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Esophageal disease can easily sneak up on the unsuspecting clinician if regurgitation, the cardinal sign of esophageal disease,
is not considered a differential diagnosis for an animal that presents for what the owner perceives as vomiting. Patients
with esophageal diseases are at risk of life-threatening complications such as esophageal perforations or aspiration pneumonitis,
so early identification of esophageal disease is important to prompt and appropriate treatment. Esophageal foreign bodies
and esophagitis have the potential, if not identified and treated, to cause esophageal strictures or megaesophagus, which
can be more difficult to treat. Failure to consider the possibility of regurgitation in the patient presented for vomiting
could lead to delays in diagnosis, treatment errors, and undesired complications. The common esophageal diseases of dogs and
cats, and the focus of these notes, are megaesophagus, esophagitis, and esophageal strictures. Less common, but still important,
causes of esophageal disease include esophageal neoplasia and gastroesophageal intussusception.
Megaesophagus
Megaesophagus can be congenital or acquired, with acquired megaesophagus a more common disease than congenital. Although
cats do develop megaesophagus, megaesophagus is seen more commonly in dogs.
Many diseases have been associated with acquired megaesophagus, and generally fall into categories of myopathies, peripheral
neuropathies, other disorders of the neuromuscular junction, or obstructive diseases such as strictures, foreign bodies, granulomas
(Spirocerca lupi) or, in younger patients with regurgitation, vascular ring anomalies. Some myopathies linked to megaesophagus include inflammatory
myopathies of infectious or non-infectious (immune-mediated) origin (polymyositis, systemic lupus erythematosis, dermatomyositis).
Some neuropathies tied to acquired megaesophagus include polyradiculoneuritis, bilateral vagal injury, dysautonomia, and lead
and thallium toxicity. Other neuromuscular junction diseases with the potential to cause megaesophagus include botulism,
tetanus and anticholinesterase toxicities (e.g. organophosphates). Central nervous system disease (e.g. brain stem lesions,
neoplasia, trauma) has also been associated with megaesophagus.
Myasthenia gravis (MG) is considered one of the most common causes of acquired megaesophagus in dogs; dogs with MG may have
megaesophagus as the only manifestation of neuromuscular junction disease, or may have more classical appendicular weakness.
Gaynor et al retrospectively studied a large number of dogs with megaesophagus to identify risk factors associated with the
disease. In their series of 136 dogs, the most common risk factor identified was MG, with other risk factors including esophagitis
and peripheral nerve disease. Despite being commonly cited as a risk factor for acquired megaesophagus, the Gaynor study
did not find any association between megaesophagus and hypothyroidism. Esophagitis is another common cause of acquired megaesophagus
in dogs; esophagitis itself can be the result of a number of other diseases.
The cardinal clinical sign of megaesophagus is regurgitation, which must be distinguished from vomiting by careful historical
investigation. Compared to vomiting, regurgitation is a passive process that is not proceeded by prodromal signs such as
lip-licking, anxiousness, and repeated heaving/retching. Regurgitation can occur minutes to hours after ingestion of food
or water. Distinction between regurgitation and vomiting in some patients can be difficult, and if there is any doubt about
whether a patient could be regurgitating, it may be prudent to assess esophageal function before pursuing causes of vomiting.
Failure to consider that a patient presented for vomiting may actually be regurgitating could lead to delays in diagnosis,
inappropriate therapy, or serious complications of untreated esophageal disease.
Animals with megaesophagus may also have difficulty swallowing, excessive salivation, pain with swallowing, or if pulmonary
aspiration has occurred, cough or alterations in respiratory rate and pattern. Vomiting may also be a component of the clinical
presentation potentially confounding the recognition of regurgitation as an element of the animal's clinical presentation;
vomiting can accompany megaesophagus if vomiting (usually chronic) has led to esophagitis. Animals with esophagitis or aspiration
may also have fever. Prolonged regurgitation is likely to lead to weight loss.
Physical examination abnormalities in patients with megaesophagus can include poor body condition, distension (which can be
dynamic) of the left ventral neck area, and fever and pulmonary crackles if aspiration pneumonitis is present. Patients with
MG may have evidence of peripheral weakness, although this will not be appreciated in all patients.
Once the problem of regurgitation is suspected, megaesophagus is often easily demonstrated on plain thoracic radiographs on
which an air (or sometimes fluid)-filled esophagus is readily seen. Occasionally, animals with megaesophagus will not have
an obvious air-filled esophagus apparent on thoracic radiographs, and esophageal hypomotility may be demonstrated during a
contrast esophagram. There is a risk of the patient aspirating contrast material during a contrast esophagram.
Once megaesophagus has been identified, revisiting the physical examination to carefully screen the patient for other signs
of neuromuscular disease can be helpful in prioritizing differential diagnoses.
