Difference between revisions of "Oesophageal Dysautonomia"
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===Pharmalogical Testing=== | ===Pharmalogical Testing=== | ||
* Topical ocular administration of dilute pilocarpine - miosis implies a postive result. However, not all dogs will respond. Response is dependent on damage to the postganglionic parasympathetic neuron that results in supersensitivity of the iris muscle dogs. | * Topical ocular administration of dilute pilocarpine - miosis implies a postive result. However, not all dogs will respond. Response is dependent on damage to the postganglionic parasympathetic neuron that results in supersensitivity of the iris muscle dogs. | ||
| − | * IV or SC administration of atropine (a parasympatholytic) | + | * IV or SC administration of atropine (a parasympatholytic) - lack of increase in heart rate implies a positive result |
* ID administration of histamine - the wheal and flare response may be dampened in those with dysautonomia | * ID administration of histamine - the wheal and flare response may be dampened in those with dysautonomia | ||
| − | |||
==Differential Diagnosis== | ==Differential Diagnosis== | ||
Revision as of 14:28, 10 August 2009
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This article is still under construction. |
Also known as Feline Key-Gaskell Syndrome and Feline Autonomic Polygangliopathy.
Part of a syndrome of generalised autonomic neuropathy. It has been observed throughout Western Europe and The United States.
Signalment
- Historically reported most frequently in cats but now also in dogs
- Usually seen in younger dogs
- No sex predisposition
- In a recent study of dogs confirmed as having dysautonomia those raised and housed in rural environments appeared to be at greater risk (56/65 dogs) for dysautonomia than dogs from the city
- Labrador Retrievers may have a breed predisposition
Description
- Degenerative lesions of the autonomic ganglia, spinal cord intermediate grey columns and sympathetic axons
- Aetiology still largely idiopathic
Diagnosis
Clinical Signs
Those of a generalised autonomic dysfuntion of the gastrointestinal and urinary tracts. Those associated with the oesophagus include:
- Regurgitation
- Megaoesophagus
- Oesophageal hypotmotility
The most frequent clinical signs associated with the syndrome are depression, anorexia, constipation, regurgitation or vomiting and incontinence (faecal and urinary) less frequently.
Physical Examination
Findings associated with the GI system include:
- Dry mucous membranes
- Intestinal distension
Radiography
Plain Radiography
Oesophageal dilatation may be observed.
Contrast Radiography
Oesophageal hypomotility may be evident on barium contrast study.
Histological Findings
Chromatolytic degeneration in autonomic ganglia, spinal cord intermediate grey columns and some sympathetic axons.
Pharmalogical Testing
- Topical ocular administration of dilute pilocarpine - miosis implies a postive result. However, not all dogs will respond. Response is dependent on damage to the postganglionic parasympathetic neuron that results in supersensitivity of the iris muscle dogs.
- IV or SC administration of atropine (a parasympatholytic) - lack of increase in heart rate implies a positive result
- ID administration of histamine - the wheal and flare response may be dampened in those with dysautonomia
Differential Diagnosis
There are few differentials on presentation of the many manifestations of the disease. However, early in the course of disease other causes of megaoesophagus need to be considered.
Treatment
Supportive
Including elevated feeding, gastrostomy tube feedings or total paranteral nutrition.
Parasympathomimetic Drugs
Some dogs may show minor improvement on initiation of for example, bethanechol, metoclopramide.
Prognosis
Guarded to poor. Recovery rates in the cat are reported as 20-40%, however this may take 2-12 months. In the dog recovery rates are lower. Despite recovery many are also left with residual impairment including intermittent regurgitation.