Clinical Diagnosis of Rhabdomyolysis without Myoglobinuria or Electromyographic Abnormalities in a Dog

SIMPLE SUMMARY: In this case report, we describe the case of a dog with a clinical diagnosis of rhabdomyolysis without myoglobinuria or EMG abnormalities. Rhabdomyolysis is a potentially life-threatening condition characterized by the breakdown of skeletal muscle fibers and the release of their contents into the bloodstream. This can lead to a range of symptoms, including weakness, muscle pain, dark urine (myoglobinuria), and, in severe cases, kidney failure. In humans and dogs, diagnosis typically involves, among other things, the measurement of creatine kinase (CK) activity, an enzyme released during muscle breakdown, and urinalysis for myoglobin, as well as imaging studies and other tests, such as electromyography (EMG). The severity of rhabdomyolysis can vary to a large degree. Prompt diagnosis and treatment are critical for a positive outcome. While myoglobinuria is a common finding in humans and dogs with rhabdomyolysis, it may not always be present. Similarly, while EMG studies can be a useful tool for detecting muscle abnormalities and assessing the extent of muscle damage, results thereof may not always be abnormal in cases of rhabdomyolysis. Therefore, the absence of EMG abnormalities and/or myoglobinuria does not necessarily rule out rhabdomyolysis in dogs. This case report underlines the importance of not ruling out rhabdomyolysis as a cause of clinical symptoms in dogs without myoglobinuria or EMG abnormalities. ABSTRACT: A 2-year-old female neutered Old German Shepherd was presented for acute non-ambulatory tetraparesis. Upon presentation to the emergency department, hematology and biochemical blood tests revealed no abnormalities aside from mildly elevated C-reactive protein levels (22.5 mg/L, reference range 0.0–10.0) and immeasurable creatine kinase (CK) activity. Neurological evaluation the next day revealed ambulatory tetraparesis, general proprioceptive deficits, mild ataxia and dubious diffuse myalgia. Withdrawal reflexes were weak on both thoracic and pelvic limbs. The CK was determined to be significantly elevated at that point (32.856 U/L, ref. range 10.0–200.0). Urinalysis revealed no abnormalities. An electromyographic (EMG) study of thoracic limb, paraspinal and pelvic limb muscles revealed no abnormalities. A magnetic resonance imaging (MRI) study of the cervicothoracic spinal cord was performed and revealed no abnormalities. A presumptive clinical diagnosis of rhabdomyolysis without myoglobinuria or EMG abnormalities was formed. Muscular biopsies were declined due to the rapid clinical improvement of the dog. A follow-up showed the progressive decline of CK activity to normal values and clinical remission of signs. A diagnosis of rhabdomyolysis was concluded based on clinical signs, consistent CK activity elevations and the response to supportive treatment for rhabdomyolysis, despite the absence of myoglobinuria and EMG abnormalities. Rhabdomyolysis should not be excluded based on the lack of EMG abnormalities or myoglobinuria in dogs.