Page 371 - WSAVA2018
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E. Robertson1
1American Board Certified Diplomate Feline Practice, Feline Vet and Endoscopy Vet Referrals, Brighton, East Sussex, United Kingdom
Clinical manifestations of oesophageal disease can include regurgitation, dysphagia, odynophagia (pain on swallowing), ptyalism, and exaggerated swallowing. Regurgitation has been defined as the passive expulsion of ingested material (food/ liquid) from the oesophagus and stimulated by local events af- fecting oesophageal structure/function. Attempts should be made to distinguish regurgitation from vomiting. In contrast to regurgitation, vomiting is often preceded by prodromal events such as vocalising, hypersalivation, retching, and abdominal contractions. In theory, this sounds simple; however, this can pose as a true clinical challenge for many practitioners due to their secretive lifestyles and also for the tendency of these patients to not uncommonly experience overlapping co-mor- bidities (e.g. ‘IBD’àvomited trichobezoaràoesophageal foreign bodyàoesophagitisàregurgitation AND vomiting). To add even more complexity, anorexia, coughing, dyspnoea, and pyrexia may also be noted as a possible sequela to oesophageal dis- ease due to aspiration of contents or even oesophageal per- foration.
It’s paramount for the practitioner to consider both the patient’s signalment and detailed clinical history/examination to assist with decision making. In 2018, astute owners have beautifully utilised digital information (i.e. smart phone videos) to assist the clinician in making a preliminary diagnosis of oesophageal dis- ease and guide diagnostic decisions.
Oesophageal Disease You’ll Likely Diagnose 2-3x/ year in Your Feline Career!
1) Oesophagitis
Clinical signs of oesophagitis usually develop within 1 to 3 days following an insult e.g. reflux from previous sedation/GA, access to caustic medications (e.g. doxycycline, clindamycin) 1-3 , previ- ous local trauma (vomition of trichobezoar), or from thermal in- jury. Nonspecific lethargy, anorexia, salivation, and vague oral discomfort may precede the onset of regurgitation. In cats, exag- gerated attempts to swallow with the head and neck extended, is often accompanied by gagging, retching, odynophagia (pain on swallowing), are often clues of oesophageal pathology.
Two published studies had evaluated the dynamics of tablet/ capsule swallowing in cats and highlighted how this phenom- enon occurs 4-6 In one study, tablet transit times showed that tablets and capsules made it to the stomach within 5 minutes post-administration 37% and 17% of the time, respectively. In the other study, capsules remained in the oesophagus for more than 4 minutes on 53% of occasions. It’s clear that oesophageal entrapment occurs commonly after tablet and capsule adminis- tration in cats, and if the tablet/capsules (or their contents) are potentially irritating to tissues, it’s easy to understand how oe- sophagitis occurs after these events. Interestingly, both of these studies demonstrated that the administration of a small amount of food or a small bolus of water after tablet/capsule administra-
tion was highly successful in promoting prompt and complete passage of tablet/capsules into the stomach.
In oesophagitis, survey thoracic radiographs are usually unre- markable except for the occasional presence of small amounts of air in the oesophagus. In some cases, the underlying cause of oesophagitis is identified (e.g., foreign body, hiatal hernia, or oesophageal mass. In cases of hiatal hernia, the displaced stom- ach may be identified as a mass in the dorsocaudal mediastinum cranial to the hiatus. Contrast oesophagrams are normal in mild cases; however, the mucosal surface may appear irregular with secondary hypomotility in severe cases. Segmental narrowing of the lumen can result from spasticity, intramural oedema, and focal indistensibility caused by inflammation, which can be diffi- cult to differentiate from a developing stricture.
Oesophagitis is usually an endoscopic diagnosis based on mu- cosal abnormalities. If gastro-oesophageal reflux is the under- lying cause of oesophagitis, lesions are most severe in the dis- tal esophagus and the gastroesophageal junction may appear wide open.
Treatment of oesophagitis:
Soft, low fat/high protein diet should as it may improve the low- er oesophageal tone and minimise delays in gastric emptying. Elevated feeding may reduce episodes. For severe cases PEG tube may be required.
Mucosal protectants
• Sucralfate suspension given PO: 100-200 mg/kg BID/TID
Gastric antacids
To reduce gastric acidity and thereby help prevent further esophageal damage during reflux
• Omeprazole: 1mg/kg PO BID (this is preferable to less potent H2 blockers)
• Ranitidine: 1-2 mg/kg PO bid/tid • Famotidine: 0.5 mg/kg sid/bid
Other drugs
• Analgesia (e.g. buprenorphine)
• Motility modifying agents (e.g. cisapride) can be of value to increase lower oesophageal sphincter tone and enhance gastric emptying, thereby reducing gastric reflux
2) Oesophageal Stricture
An oesophageal stricture should be suspected when regurgi- tation develops 1-4 weeks post potential suspect oesophageal injury. Clinical signs are similar to, and often impossible to differ- entiate from, oesophagitis. The appetite is often good, or even considered ravenous.
Strictures may be single or multiple. Oesophagoscopy +/- fluo- roscopy are the most reliable method(s) for diagnosing oesoph- ageal stricture(s) and also for determining the lumenal diameter, stricture length, and presence of associated oesophagitis. Sin- gle strictures are found in 80% of patients, but diffuse oesopha- gitis can result in 2 or 3 strictured areas in some cases. Management can include endoscopically guided balloon dila- tation7, or rarely, a stent8. The balloon catheter can be passed through the lubricated operating channel of many endoscopes or guided alongside the endoscope to visualize the breaking down of fibrous tissue in a controlled manner. The procedure is repeated at 3 to 5 day intervals for a minimum of three treat- ments. The total number of dilatations is variable (averaging four
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