A 3-year-old 2.5-kg (5.5-lb) sexually intact male Pomeranian was evaluated because of non–weight-bearing lameness of the right forelimb of 1 day's duration that developed after falling from its owner's bed. On physical examination, the only abnormality was signs of pain localized to the proximal portion of the right antebrachium. Results of a CBC and serum biochemical analysis revealed no clinically relevant abnormalities.
The patient was sedated with methadone (0.4 mg/kg [0.18 mg/lb], SC) and acepromazine (0.05 mg/kg [0.023 mg/lb], SC). Anesthesia was induced with propofol (4 mg/kg [1.8 mg/lb], IV) and thiopentone (4 mg/kg, IV) and maintained with isoflurane in oxygen at a concentration of 1% to 2% after orotracheal intubation.
Orthogonal radiographs of both antebrachia were obtained. The proximal portion of the right radius had a minimally displaced, reducible fracture that appeared to have propagated from a well-demarcated, ovoid, osteolytic lesion within the cortex of the caudolateral aspect of the radius (Figure 1). The right ulna, left radius, and left ulna were unremarkable. Subsequently, the right forelimb was further assessed with CT.a Computed tomography confirmed the fracture, and its communication with an expansile, osteolytic lesion and the associated smooth periosteal reaction of the caudolateral aspect of the proximal diaphysis of the radius (Figure 2). No abnormalities were noted on CT images of the contralateral radius, shoulder and elbow joints of both forelimbs, thorax, and abdomen. Imaging results were consistent with RUIN and secondary fracture of the radius. Plans were then immediately made to biopsy the bony lesion and repair the fracture by open reduction and internal fixation. Cefazolin (22 mg/kg [10 mg/lb], IV) was administered to the patient prior to proceeding with surgery.
Craniocaudal (A) and mediolateral (B) radiographic views of the right antebrachium of a 3-year-old 2.5-kg (5.5-lb) sexually intact male Pomeranian examined because of right forelimb lameness of 1 day's duration. Note the fracture of the radius at the approximate junction of the proximal and middle thirds of its diaphysis (arrowheads) and the well-demarcated, ovoid, osteolytic lesion (black arrow) with cortical bone loss and smooth periosteal reaction (white arrow) on the caudolateral aspect of the radius in close association with the fracture line.
Citation: Journal of the American Veterinary Medical Association 257, 4; 10.2460/javma.257.4.406
Computed tomographic images of the right antebrachium of the dog in Figure 1 in the sagittal plane (A) and in a transverse plane at the approximate junction of the proximal and middle thirds of the diaphysis (B). Note the fracture line (black arrow; A) communicating with an expansile (black arrowheads; A), osteolytic lesion (white arrow; A and B) at the caudolateral aspect of the radius.
Citation: Journal of the American Veterinary Medical Association 257, 4; 10.2460/javma.257.4.406
The patient was positioned in dorsal recumbency, and the right forelimb was clipped of hair and aseptically prepared for surgery. The limb was draped, and a craniomedial approach to the right radius was made. The fracture was visualized, and the lateral surface of the radial cortex appeared expanded (Figure 3). A tenacious, rubbery fibrous tissue filled the gap between the fracture fragments. A bone curette was used to remove this tissue as well as open the proximal and distal portions of the medullary cavity. The tissue was placed into a container of neutral-buffered 10% formalin and submitted for histologic examination. Then, the fracture was reduced with bone reduction forceps. A 7-hole locking bone plateb was contoured, applied to the cranial aspect of the radius, and secured with 6 bicortical locked screws, with 3 each proximal and distal to the fracture line, such that the middle hole of the plate immediately adjacent to the fracture remained open. A locking screw was also placed to hold the fragments in approximate reduction (Figure 4). During surgery, methadone (0.3 mg/kg [0.14 mg/lb], IV) was administered, and cefazolin (22 mg/kg, IV) was read-ministered once 90 minutes after administration of the first dose and then every 6 hours for 2 doses. Postoperative radiography confirmed reduction and stabilization of the fracture. The patient recovered uneventfully from anesthesia and was discharged from the hospital 1 day after surgery with a 7-day supply each of cephalexin (22 mg/kg, PO, q 12 h) and meloxicam (0.1 mg/kg [0.045 mg/lb], PO, q 24 h). The owner was instructed to restrict the patient's activity to short walks on a leash for 6 weeks.
Intraoperative photograph of a portion of the diaphysis of the right radius of the dog in Figure 1. The distal portion of the radius is to the top and the proximal portion of the radius is to the bottom of the image. Note the fibrous tissue within the gap between the fracture fragments (arrow).
Citation: Journal of the American Veterinary Medical Association 257, 4; 10.2460/javma.257.4.406
Radiographs of the right antebrachium of the dog in Figure 1 obtained immediately after surgery. The fracture was stabilized with a bone plate and a positional screw.
Citation: Journal of the American Veterinary Medical Association 257, 4; 10.2460/javma.257.4.406
Sections of the harvested fibrous tissue were processed normally and stained with H&E stain, and histologic examination revealed the presence of viable bone associated with dense fibrous tissue. A large proportion of the fibrous tissue was anuclear and had small areas of coagulative necrosis. No neoplastic cells were identified, and no bacteria or fungal elements were identified with a second histologic examination of tissue stained with special stains.
On physical examination 12 days after surgery, the patient ambulated normally with the right forelimb and did not have signs of pain on palpation of the surgical site. Fifteen weeks after surgery, the dog continued to ambulate normally, and findings on radiographic and CT examinations of the right antebrachium indicated healing at the fracture site and remodeling of the bone associated with the RUIN lesion (Figure 5).
Radiographs of the right antebrachium of the dog in Figure 1 obtained 15 weeks after surgery. Note healing and remodeling of the bone associated with the fracture and RUIN lesion.
Citation: Journal of the American Veterinary Medical Association 257, 4; 10.2460/javma.257.4.406
Discussion
To our knowledge, RUIN has been reported in only 1 dog.1 Ischemic necrosis of bone refers to the death of the cellular constituents of bone secondary to impairment of the blood supply. Although the etiology and pathogenesis of RUIN have yet to be established,1 the histologic changes of the radius in the dog of the present report were likely secondary to ischemia. Chronic disease was supported by the radiographic and histologic findings, which are similar to those observed with other ischemic and necrotic diseases of bone.2–5
A thick interosseous ligament occupies the space between the apposed surfaces of the radius and ulna, starting immediately distal to the radioulnar joint and extending slightly beyond the midpoint of the length of the ulna.6,7 The nutrient arteries of the radius and ulna arise from the caudal interosseous artery and are the principal blood supply to the diaphyseal cortices of the radius and ulna. For each bone, the nutrient arteries enter the bone through the nutrient foramen at the junction of the proximal and middle thirds of the diaphysis, although variation to this location is possible.8,9 The nutrient arteries do not branch when traversing the cortex through the foramen but instead branch on exiting into the medullary cavity to supply blood to two-thirds of the shaft of the bone.10,11 For the dog of the present report, RUIN of the radius was located at the level of the nutrient foramen and the interosseous ligament; therefore, disruption to the blood supply at the level of the nutrient foramen of the radius may have precipitated necrosis and subsequent fracture.
Possibly, enthesopathy of the interosseous ligament precipitated RUIN by disrupting the blood flow by periosteal arterioles or branches of the nutrient arteries to the bone. Enthesopathy of the interosseous ligament at the caudal aspect of the radius is common but can differ in appearance, including as irregular cortical margination, endosteal sclerosis, and osteolysis.1,12 Authors of the other report1 of the dog with RUIN specified an insertion desmopathy, as determined by the presence of enthesophytes along the radioulnar insertion zone of the interosseous ligament. Additionally, Deffontaines et al7 describe radioulnar desmitis and enthesophytosis as the causes of chronic forelimb lameness in a young Labrador Retriever. However, the dog of the present report did not have chronic forelimb lameness and radiographic and CT evidence of enthesophytes; therefore, RUIN secondary to an enthesopathy was unlikely. Angiography of dogs with RUIN could be performed to confirm whether disruption of the blood supply to the bone is the cause of RUIN. However, angiography is invasive; therefore, its use is limited in clinical practice.
Forelimb lameness and focal osteolysis of cortical bone and a smooth periosteal reaction between the proximal and middle thirds of the diaphysis of the radius or ulna in dogs should prompt veterinarians to include RUIN as a differential diagnosis. The present report described a dog with RUIN, which manifested as acute right forelimb lameness after trauma-induced fracture of the radius. Lameness and the RUIN lesion resolved with debridement and fracture repair by open reduction and internal fixation. The patient ambulated normally 12 days after surgery and continued to do so 15 weeks after surgery, suggesting that the prognosis for dogs with RUIN may be good with surgical intervention.
Acknowledgments
The authors thank Dr. Richard Lam for providing his expertise in CT imaging and manuscript preparation.
No external funding was provided. The authors declare that there were no conflicts of interest.
Presented in abstract form at the Science Week Conference of the Australian and New Zealand College of Veterinary Scientists, Surfers Paradise, QLD, Australia, July 2018.
ABBREVIATIONS
| RUIN | Radioulnar ischemic necrosis |
Footnotes
Brilliance 6, Philips Healthcare, Macquarie Park, NSW, Australia.
Intrauma SpA, Genova, Italy.
References
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