Page 483 - Small Animal Internal Medicine, 6th Edition

CHAPTER 29 Disorders of the Oral Cavity, Pharynx, and Esophagus 455

(even if serum electrolyte concentrations are normal; see ESOPHAGITIS
Chapter 50). Electromyography may reveal generalized neu- Etiology
VetBooks.ir ropathies or myopathies. Dysautonomia occurs occasionally Esophagitis is principally caused by gastroesophageal reflux,
and is suspected on the basis of clinical signs (i.e., dilated
persistent vomiting of gastric acid, esophageal foreign
colon, dry nose, dilated pupils, keratoconjunctivitis sicca,
and/or bradycardia that responds poorly to atropine). Gastric objects, and caustic agents. Medicines, especially tetracy-
outflow obstruction in cats can cause intractable vomiting clines, clindamycin, ciprofloxacin, and nonsteroidal antiin-
with secondary esophagitis producing megaesophagus. flammatory drugs (NSAIDs) may cause severe esophagitis if
Other causes are rarely found (see Box 26.5). If an underlying they are retained in the esophagus because they are not
cause cannot be found, the disease is termed idiopathic washed down with water or food (especially in cats).
acquired esophageal weakness (i.e., idiopathic acquired Gastroesophageal reflux during anesthesia can produce
megaesophagus). severe esophagitis with subsequent stricture formation. It is
impossible to predict which animals will reflux during anes-
Treatment thesia. Various factors have been suggested to place patients
Dogs with acquired megaesophagus caused by hypoad- at increased risk for anesthesia-associated reflux, but none
renocorticism typically respond well to glucocorticoid has consistently had a strong association that can be used
replacement (see Chapter 50). Localized myasthenia typi- clinically. An association between distal esophagitis (ostensi-
cally responds to pyridostigmine, which is preferred to bly caused by gastroesophageal reflux) and upper respiratory
physostigmine and neostigmine (see Chapter 66). Adjunc- disease in brachycephalic dogs has been suggested. Eosino-
tive immunosuppressive therapy with azathioprine may be philic esophagitis is rare and has uncertain causes in dogs.
helpful in some patients not responding well to pyridostig- Pythiosis can cause severe esophagitis (see p. 484).
mine, but it is not clear that combination therapy is always
superior to pyridostigmine alone. Glucocorticoid therapy is Clinical Features
not recommended. Gastroesophageal reflux may respond Signs depend upon the severity of the inflammation. Regur-
to prokinetic and antacid therapy (cisapride at 0.1-0.5 mg/ gitation is expected, although anorexia and drooling due to
kg PO q8-12h and omeprazole at 1-2 mg/kg PO q12h are refusal to swallow may predominate if swallowing is too
preferred). If the disease is idiopathic, conservative dietary painful. If a caustic agent (e.g., disinfectant) is ingested, the
therapy as described for congenital esophageal weakness is mouth and tongue are often hyperemic and/or ulcerated;
the only recourse. Some dogs with congenital esophageal hyporexia may be the primary sign.
weakness regain variable degrees of esophageal function,
but this is less common with idiopathic acquired esophageal Diagnosis
weakness. Severe esophagitis may cause secondary esopha- A history of vomiting followed by a change in character that
geal weakness, which resolves after appropriate therapy sounds more like regurgitation suggests esophagitis second-
(discussed in more detail later in this chapter). In severely ary to excessive exposure to vomited gastric acid (e.g., dogs
affected patients not responding adequately to dietary/ with parvoviral enteritis or foreign body obstruction).
feeding modifications, gastrostomy tubes may diminish the Regurgitation or hyporexia beginning shortly after an anes-
potential for aspiration, ensure positive nitrogen balance, thetic procedure may indicate esophagitis caused by reflux.
and allow for administration of oral drugs. Some dogs Plain and contrast radiographs may reveal hiatal hernias,
benefit from the long-term use of a gastrostomy tube, but gastroesophageal reflux, or esophageal foreign bodies. Con-
others continue to regurgitate and aspirate due to severe trast esophagrams do not reliably detect esophagitis (some-
gastroesophageal reflux or accumulation of saliva in the times there is slight barium retention by the roughed,
esophagus. irregular mucosa), but contrast enhanced fluoroscopy can be
definitive for gastroesophageal reflux in some cases (Video
Prognosis 29.3). Typically esophagoscopy is needed to diagnose esoph-
All animals with acquired esophageal weakness are at agitis (Fig. 27.11).
risk for aspiration pneumonia and sudden death. If the
underlying cause can be treated and the esophageal dila- Treatment
tion and weakness can be resolved, the prognosis is often Decreasing gastric acidity, preventing reflux of gastric con-
good because the risk of aspiration is eliminated. The prog- tents into the esophagus, and protecting the denuded esoph-
nosis is worse in patients with aspiration pneumonia and agus are the hallmarks of treatment. Proton pump inhibitors
those with idiopathic megaesophagus that are older than (e.g., omeprazole) are far superior to histamine-2 (H 2 ) recep-
13 months of age at the time of onset of clinical signs tor antagonists for decreasing gastric acidity, a critical factor
because they are less likely to experience spontaneous in these animals. Metoclopramide stimulates gastric empty-
remission. The prognosis is also poor for patients that fail ing, resulting in less gastric volume to reflux into the esopha-
to respond to dietary/feeding management. The size of the gus; its main advantage is that it can be given intravenously.
esophageal dilation on radiographs is not clearly associated Cisapride (0.1-0.5 mg/kg) is a more effective prokinetic but
with prognosis. must be given orally. Erythromycin and ranitidine also have