NEUROMUSCULAR CASE OF THE MONTH - JANUARY 2012
Resolution of megaesophagus in an adult female mixed breed dog after treatment of concomitant hypothyroidism
Contributed by Dr. Edouard Huber
Clinique vétérinaire Les Grillières
Montcherand, CH, 1354 (Switzerland)
An adult mix breed female hunting dog of 40kg was presented with a two month history of regurgitation and vomiting bile. Previous treatments
included domperidon, cimetidine, and clindamycin which did not result in clinical improvement.
The dog was obese, weak, and lethargic with generalized muscular atrophy. The hair coat was lusterless and a slight dry seborrhea
and diffuse ventral alopecia were noted. Vital signs were normal. Cranial and spinal nerve evaluations were considered normal. The
dog regurgitated during the examination. Regurgitation secondary to megaesophagus and possibly hypothyroidism were suspected.
|| (6-12 X 109/l)
|| (2.84-8.27 mmol/l)
| Alk Phosphatase
|| (1.3-3.7 µg/100ml)
| Canine TSH
|| (0-0.32 ng/ml)
| Free T4
|| (9-33 µmol/l)
| AChR antibody
Based on the results of laboratory testing and the presence of esophageal dilatation on thoracic radiographs, a diagnosis of generalized
acquired megaesophagus possibly associated with hypothyroidism was made. A diagnosis of acquired myasthenia gravis was thought to be
unlikely since the acetylcholine receptor antibody titer (AChR antibody) was negative.
Figure 1. Thoracic radiographs- Marked, generalized megaesophagus
Treatment and Clinical Outcome
L-thyroxin was initiated at 20µg/kg twice daily and enrofloxacin at 5mg/kg for10 days in order to prevent a possible
pulmonary infection secondary to aspiration. Mestinon therapy, initiated prior to receiving results of the AChR antibody testing,
was stopped following receipt of the negative titer. One month later, the dog was alert, active, and regurgitation had ceased.
The dog had lost 3kg in body weight. Thoracic radiographs showed the megaesophagus had markedly diminished (about 60%). The
thyroxin blood level was too high at 5.3µg/100ml so the dosage of L-thyroxin was decreased to 20µg/kg daily. Over
the following month the thyroxin level became normal (2.4µg/100ml). Eleven months later, the vitality and the general
health status was still very good and the dog had a normal weight of 32kg. The hair coat was bright and full. Repeat thoracic
radiographs showed complete resolution of the megaesophagus (Figure 2. ). The thyroxin level was within normal range. Two years
later, the dog is still receiving L-thyroxin supplementation and is doing very well without reoccurrence of megaesophagus.
In a retrospective study of 29 dogs with neurologic signs and hypothyroïdism (1), 4 dogs suffered from a concomitant megaesophagus.
At long term (16 months), 1 dog showed clinical and radiological resolution, 2 dogs improved with occasional episodes of regurgitation,
and 1 dog was euthanitized because of worsening of clinical signs. Hypothyroïdism could initiate a metabolic myopathy or neuropathy
associated with a megaesophagus. On the other hand, hypothyroïdism and megaesophagus could be the simultaneous expression of two
distinct immune mediated disorders: thyroïditis and an immune mediated neuropathy. In a prospective study of risk factors leading
to megaesophagus (2), a causal relationship between megaesophagus and hypothyroidism could not be demonstrated. In this case, the complete
resolution of the megaesophagus and other clinical signs of hypothyroidism following therapy with L-thyroxin is highly suggestive of
but does not prove a causal relationship between megaesophagus and hypothyroidism.
1. Jaggy A., Oliver J.E., Ferguson D.C., Mahaffey E.A., Glaus T. Neurological manifestations of hypothyroidism: a retrospective study
of 29 dogs. J. Vet. Int. Med. 1994, 8:328-336
2. Gaynor A.R., Shofer E.S., Washabau R.J. Risk factors for acquired megaesophagus in dogs. J. Am. Vet. Med. Assoc. 1997, 211 : 1406-1412
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