Clinical History
A 4 year old Golden retriever presented to the referring veterinarian for a one day history of collapsing episodes. No health problems were reported by the owner prior these episodes. The owner did report that the dog may have been slowing down and possibly weaker over the past few months, but it had also gained 15 pounds. As far as could be determined there was no exposure to toxins, vaccination status was up to date, and it received regular heartworm prevention. The dog was playing in the owner’s yard when it suddenly started running in a circle (Go to video 1), collapsed, and could not rise. Shortly after this, it was again able to walk, and then suddenly started circling in the other direction (Go to video 2), collapsed again and was unable to walk without support. The dog was then taken to the referring veterinarian where it was treated with intravenous diazepam for suspected “seizure” activity, then transferred to the Veterinary Teaching Hospital emergency service at LSU. 

Physical Examination
On presentation the dog was not able to walk by itself and appeared weak when supported. A tremor was observed in the left thoracic limb. All vital parameters were within the normal limits with the dog fully responsive and mentally appropriate. Body condition score was estimated at 8/9. Neurologic examination revealed a normal mental status and cranial nerves, normal papillary light reflexes and normal proprioception and placing. Spinal reflexes were weak to absent. No spinal or neck pain was detected. A neuromuscular disorder was suspected.

Emergency Diagnostics
Arterial blood gas analysis: No abnormalities
CBC: No abnormalities
Chemistry Panel: AST 367 U/L (reference 2-38), CK >2000 U/L (reference 67-200)
Coagulation Panel: PT and PTT within the reference range
Thoracic and abdominal radiographs: No significant abnormalities

Further Physical Examination
The dog was hospitalized and monitored in ICU for “seizure” activity without any episodes. Treatment was limited to fluid therapy to prevent dehydration. The following morning the dog was bright, alert and responsive with a normal physical examination. It was able to rise with no obvious gait abnormalities. However, during a 20 minute walk, the dog became progressively slower and then collapsed, and was unable to rise. Discomfort was detected on manual palpation of the muscles, and when the joints were flexed and extended. Patellar reflexes were absent bilaterally and withdrawal reflex was weak in all limbs.

Diagnostic Testing
Muscle enzymes after exercise and collapse: AST 466 U/L, CK 11,163 U/L
Thyroid panel: Did not support hypothyroidism
Antibody titers for infectious disease: Negative for Neospora caninum, Toxoplasma gondii, Babesia canis, Rickettsia rickettsii and Borrelia burgdorferi. The antibody titer for Ehrlichia canis was positive at 1:160
Acetylcholine receptor antibody titer: within the reference range
EMG: Spontaneous activity consistent with muscle disease
Muscle and Nerve biopsies: Biopsies were collected under general anesthesia from the triceps, cranial tibial, biceps femoris and extensor carpi radialis muscles. Myonecrosis (see below, H&E stain) was present in all muscles. Infiltrating cells were predominantly macrophages and were in appropriate numbers for the degree of muscle degeneration. No organisms were observed. A biopsy from the common peroneal nerve was normal.

Diagnosis and Treatment
A necrotizing myopathy of undetermined origin was diagnosed. On day 2 following presentation, treatment was initiated with L-thyroxin, clindamycin and tramadol. L-thyroxin was discontinued on day 7 after the results of the thyroid panel were received. Tramadol and clindamycin were discontinued on day 8 following receipt of the negative antibody titers for infectious diseases. Doxycycline was initiated, as the antibody titer for Ehrlichia canis was positive, and continued for 4 weeks.

Outcome
Recovery was complete within a few days. Due to the request of the owner, the dog remained hospitalized for 10 days receiving physical and neurological examinations twice daily. On days 7-9, leash walks were initiated, and even after walking and running for 30 minutes, no episodes of collapse or weakness occurred. Myalgia was not detected. The CK returned to the reference range. Eight weeks after discharge the dog was still asymptomatic. While the cause of the acute myopathy was not determined, toxic exposure or reaction to an inset bite were discussed as possibilities. Ehrlichia canis infection was deemed unlikely as the cause of the myopathy, however treatment with doxycycline was given for 4 weeks. A repeat thyroid panel and gradual weight loss was recommended to the owners.

For a review of necrotizing myopathies and possible causes see Shelton GD. Rhabdomyolysis, myoglobinuria, and necrotizing myopathies. Vet Clin North Am Small Anim Pract 2004;34:1469-1482.