NEUROMUSCULAR CASE OF THE MONTH - FEBRUARY 2006

Necrotizing Myopathy in the Biceps Femoris Muscles of a 11 yr old FS Greyhound
Contributed by Dr Peter Brofman
Veterinary Speciality Hospital
Cary, NC 27511



Clinical History
A left thoracic limb amputation resulting from trauma had been performed several years prior to the current problem. Two  months prior to admission, the  dog presented  to another veterinarian for acute onset of pelvic limb paresis that was unchanged for 2 weeks. Examination at that time revealed a minimally ambulatory pelvic limb paresis with  intact  reflexes and caudal lumbar hyperpathia. Blood work, including a CBC and serum chemistry analysis (did not include a CK), was normal.  Following an epidural injection of Depo-Medrol, the dog was reported to be ambulatory within 24 hours. Recheck with the veterinarian 2 weeks later revealed the dog had a short stride in the left pelvic limb and left coxofemoral joint pain, but no spinal  hyperpathia. The dog then presented 2 months later to the Veterinary Specialty Hospital (VSH) for a similar episode of acute onset of pelvic limb paresis.

Physical and Neurological Examination
Abnormalities were limited to the neuromuscular system and included a left pelvic limb lameness. Other than an absent cutaneous trunci reflex on the left, no neurologic deficits were found. There was pain over the gluteal and thigh muscles bilaterally.

Diagnostic Testing

MRI: An MRI was performed to evaluate the thoracolumbar spine and pelvic limb musculature. The thoracolumbar spine was normal. Imaging of the pelvic limbs demonstrated T2 hyperintensity in both biceps femoris muscles and in the right gluteal muscle (Fig. 1A). T1 images with fat saturation also demonstrated hyperintensity within the same areas (Fig. 1B), suggesting the  presence of methemoglobin. Following the intravenous administration of gadolinium, there was heterogeous enhancement of these lesions, with a well defined peripheral enhancement and absence of enhancement centrally, suggesting avascular or necrotic regions. The appearance of the images was consistent with myositis or myonecrosis, but hemangiosarcoma could not be ruled out.


1A

1B

Fine needle aspirate of biceps femoris muscle: Neutrophilic/histiocytic inflammation with a spindle cell proliferation 

Surgical biopsy of the biceps femoris muscle: Both biceps femoris muscles were pale in color and firmer than the surrounding muscle. Impression smears of the biopsies demonstrated necrosis and mixed inflammation with erythrophagocytosis. Biopsies from both the right and left biceps femoris muscles were evaluated in frozen sections and similar changes were present within both muscles (Fig. 2). Numerous myofibers were at a similar stange of necrosis and phagocytosis. Overt lymphocytic infiltration was not  present. No organisms were observed.

.


2

Tissue culture: Negative
Antibody titers for Rocky Mountain Spotted Fever, Lymes disease, Ehrlichia, Toxoplasma and Neospora: Negative
T4: 0.7 (1-4mg/dl)
CK: 46 (59-895 IU/L)
Coagulation profile with D-dimer: Normal

Diagnosis and Outcome
An intermittent interruption of the vascular supply to the biceps femoris and gluteal muscles resulting in tissue ischemia was suspected. Myonecrosis would be the end result of such interrupted vascular supply. The dog was treated with Tramadol (75 mg PO three times daily) and Clindamycin (300 mg PO twice daily) and clinically was markedly improved 2 weeks following evaluation.

 

 


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