Vet360 Vet360 Vol 05 Issue 04 - Page 24

GASTRO-ENTEROLOGY Sialoadenosis has a major clinical impact and is often misdiagnosed as nausea. The following two articles aim to demystify the condition Sialoadenosis and Limbic Epilepsy Liesel van der Merwe BVSc MMed Vet (Med) Small Animals Senior Lecturer, Outpatients OVAH Sialoadenosis is a bilateral, persistent, painless, soft, non-neoplastic, non-inflammatory swelling usually involving the parotid and sometimes also the mandibular salivary glands. Salivary gland enlargement is an uncommon condition in dogs. In a review of 245 salivary gland biopsies from animals, salivary glands accounted for only 0.3% of all biopsies received. The majority of these biopsies (65%) were obtained from dogs and demonstrated neoplasia (30%), inflammation (29%), sialocoele formation (11%), infarction (9%), with the remainder showing miscellaneous changes. Hypersialosis or ptyalism is excessive secretion of saliva (true hypersialosis) or inability to contain saliva within the oral cavity, as may occur with dysphagia. Ptyalism also occurs secondary to both stimulation of salivary secretion caused by other disorders (e.g. dysphagia) and primary disease of the salivary gland (e.g. sialadenosis). Sialorrhoea, ptyalism or hypersialosis are synonyms used to describe the excessive production of saliva. Sialoadenosis causes clinical signs of retching, gulping, anorexia, nausea, vomiting and sialorrhoea with firm palpable, often enlarged salivary glands in dogs. If endoscopic evaluation of the stomach and oesophagus reveals no lesions and there is no histological evidence of gastritis or oesophagitis, and thoracic imaging reveal no extraluminal oesophageal pathology, a diagnosis of idiopathic phenobarbitone- responsive hypersialosis can be made. The terrier breeds, especially fox terriers and Jack Russell terriers, are over-represented in the literature for both secondary and idiopathic sialorrhoea. It is suggested that all forms of human sialoadenosis are caused by degenerative changes demyelinating polyneuropathy,in the autonomic nervous system. vet360 Issue 04 | SEPTEMBER 2018 | 24 Salivary gland enlargement may be a secondary reactive change because of over-stimulation by the parasympathetic system. Three publications reported that surgical resection of the affected salivary glands, failed to stop the hypersalivation and dysphagia until phenobarbitone was administered to the patients. This finding supports the theory that the sialorrhoea is part of a multifactorial parasympathetic response to an underlying stimulus or condition. It has been suggested that the idiopathic form of the disease may be a form of epilepsy, namely limbic epilepsy.The sialorrhoea and oral discomfort (odynophagia) exhibited by these patients responds well to phenobarbitone. There is no direct evidence linking phenobarbitone to saliva production but it does reduce small intestinal motility and could have local effects on the salivary glands The effectiveness of the phenobarbitone may indicate that the primary cause of the condition is parasympathetic activation of salivary gland secretion. The exact mechanism of action of phenobarbitone is unknown, but is likely to involve inhibition of excitatory neurotransmitters, such as glutamate, and a gamma aminobutyric acid mimetic effect. Successful therapeutic intervention using anticonvulsants for sialoadenosis in dogs was first demonstrated in 1979 by Kelly et al. using phenytoin and primidone and subsequently, phenobarbitone was successfully used in several small case series. Most dogs improved within 48 h and all improved within 4 days. In the largest case series described, a starting oral dose of 1 mg/kg PO q12h was effective, although others have used higher doses (2–3 mg/ kg PO q12h), suitable for control of idiopathic epilepsy, with and without a loading dose. In one-quarter of the cases, tapering and cessation of phenobarbitone therapy was possible after a variable length of time (6–12 months until cessation). References 1. Boydell, P., Pike, R., Crossley, D. & Whitbread, T., 2000a, ‘Sialadeno- sis in dogs’, Journal of the American Veterinary Medical Association 216, 872–874. 2. Brooks, D.G., Hottinger, H.A. & Dunstan, R.W., 1995, ‘Canine nec- rotizing sialometaplasia: A case report and review of the literature’, Journal of the American Animal Hospital Association 31, 21–25. 3. Chapman, B.L. & Malik, R., 1992, ‘Phenobarbitone-responsive hypersialism in two dogs’, Journal of Small Animal Practice 33, 549–552. 4. Cooke, M.M. & Guilford, W.G., 1992, ‘Salivary gland necrosis in a wire-haired fox terrier’, New Zealand Veterinary Journal 40, 69–72. 5. Gibbon, K.J., Trepanier, L.A. & Delaney, F.A., 2004, ‘Phenobarbitone responsive ptyalism, dysphagia and apparent esophageal spasm in a German shepherd puppy’, Journal of the American Animal Hospital Association 40, 230–237. 6. Kelly, D.F., Lucke, V.M., Denny, H.R. & Lane, J.G., 1979, ‘Histology of salivary gland infarction in the dog’, Veterinary Pathology 16,