A 3yo ME Collie-cross farm-dog went missing for several hours during a walk, returning fairly exhausted and on a hot day, and was cooled off in the pond due to concern for heat stress. At presentation the following day a stiff gait was noted and there was generalised weakness and discomfort on palpation and manipulation of both the fore- and hind-limbs. He was also noted to be slightly pale, and temperature was 39.7oC
- His owner also provides a urine sample that they collected from the dog at home.
- What are the most common causes of abnormal urine colour in dogs?
- What further testing would you recommend in this case
Urine discolouration may occur for a variety of reasons, but the most common causes result from haematuria, haemoglobinuria, myoglobinuria and bilirubinuria.
Haematuria may be differentiated from pigmenturia by spinning down urine to see if the discolouration clears, and in combination with sediment examination to look for whole red blood cells. Clearance of the discolouration, and the absence of whole RBCs on sediment examination would exclude haematuria, and be compatible with pigment. In this dog’s case, pending the results of biochemistry and haematology urine was spun and the pigment did not clear. Sediment examination also did not identify red blood cells, which made pigmenturia (haemoglobinuria, myoglobinuria, bilirubinuria) more likely.
A spun plasma sample did not identify haemolysis, and haematology ultimately did not identify anaemia despite the pale mucous membranes on physical examination. This excluded haemoglobinuria due to pre-renal RBC haemolysis, but not RBC lysis within the urine itself. However the gait stiffness and limb discomfort was considered more likely to represent myalgia, and therefore myoglobinuria was felt to be more likely.
When biochemistry results were available, a markedly elevated creatinine kinase (CK) result was found that was above the machine’s readable value. Other biochemistry parameters, including bilirubin, were normal allowing us to exclude bilirubinuria.
The Internal Medicine Team at VetCT discussed these combined findings with the primary care vet, and consulted our Neurology Team as well for additional management advice. Together the clinicopathologic findings were felt to be most compatible with rhabdomyolysis. Rhabdomyolysis results from uncontrolled intracellular calcium increases within myofibres, with release of calcium-dependent proteases that subsequently result in myonecrosis.
With the reported history the most likely cause was felt to be exertional rhabdomyolysis following more extreme exercise. Other differentials would include toxin or venom exposure, and less likely for this case based upon history and examination, drug reactions and infectious process. Genetic defects resulting in disturbances in glycogen or lipid metabolism, mitochondrial dysfunction or in spontaneous intramuscular calcium release might be considered where there was repeated presentation. However these conditions are rare in dogs.
Management in this case included intravenous fluid therapy to protect the kidneys from risk of an acute kidney injury, and this was recommended to continue until such time that the magnitude of pigmenturia dramatically reduced and the risk of AKI was therefore minimal. Monitoring of urea, creatinine concentrations was also discussed. As CK has a short half-life this was also suggested to be useful as a marker of resolution of myonecrosis. Pain management with opioids was also recommended.
Our neurology team also considered exertional rhabdomyolysis most likely and in addition to the above recommended supplementation with Co-enzyme Q10, L-Carnitine and riboflavin (or B-complex vitamin supplements) to aid recovery, together with gentle passive range of motion physiotherapy.
The dog was discharged 48 hours later after a marked clinical improvement.
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