Hypertrophic Osteodystrophy of the Proximal Humerus in Two Dogs
Two dogs, 3 and 6 months of age, were presented with painful, swollen shoulder and carpal joints; reluctance to stand; and pyrexia. Radiographs in both cases revealed an irregular lucent zone in the metaphysis of the proximal humerus, parallel and adjacent to the physis. The same lucent zone was also evident in the physes of the distal radial and ulnar metaphyses. Clinical signs and radiographs were consistent with hypertrophic osteodystrophy. Clinical signs resolved in both dogs with administration of carprofen, tramadol, and intravenous fluids. No signs of recurrence were reported at 3-month follow-ups.
Introduction
Hypertrophic osteodystrophy is a systemic disease that primarily affects skeletally immature large- and giant-breed dogs, but it has also been reported in a toy breed.1 The onset of clinical signs has been reported as early as 7 weeks with an average of 3 to 5 months, and relapses may occur as late as 8 months of age.2–4 The disease is sporadic, and males seem to be more commonly affected than females.4–7 Typically, dogs with hypertrophic osteodystrophy are presented after a brief period of mild lameness and an acute onset of moderately painful, soft-tissue swellings over the distal forelimbs and hind limbs.3 The pain is thought to arise from periosteal capillary hemorrhage with irritation of periosteal nerve endings.8 Depending on the severity of the disease, clinical signs may include varying degrees of lameness, marked pyrexia (40°C or higher), painful metaphyseal regions, footpad hyperkeratosis, anemia, diarrhea, and pneumonia.5,9,10 Hematological and serum biochemical values may reveal leukocytosis, but results are usually normal.5
Abnormalities in the metaphyseal region of long bones, immediately adjacent to the physis, are generally bilaterally symmetric.2,8,9 Disturbance of metaphyseal blood supply is reported to lead to changes in the physis and adjacent metaphyseal bone, resulting in a delayed ossification of the physeal hypertrophic zone of the physis.4 Radiographic abnormalities are commonly seen in the distal radius, ulna, and tibia.2,3,8,9 The radiographic hallmark of hypertrophic osteodystrophy is an irregular radiolucent zone in the metaphysis that is separated from the physis by a dense band.3–5,8–10 The mandible, metacarpal and metatarsal bones, costochondral ribs, scapula, and the vertebrae are less commonly involved.2,5–10
Many investigators have speculated on the etiology of hypertrophic osteodystrophy, but little scientific data exist to support the proposed etiologies. No single agent or disorder has been proven to cause or reproduce the disease.8 Possible causal factors include over-supplementation of minerals, vitamins, and dietary protein; hypovitaminosis C; and suppurative inflammation without isolation of infectious agents.8–10 More recently, a link to canine distemper virus has also been postulated.4,6,9,10 Although bacteremia has been reported to be concurrent with hypertrophic osteodystrophy, no causative microorganisms have been isolated or observed histopathologically in the bones of dogs with hypertrophic osteodystrophy.2,5,10 Although cases have been reported in littermates, no mode of inheritance has been suggested.8
Typically, the disease is self-limiting and resolves after a few weeks. However, severe disease or multiple relapses can ultimately result in abnormal/premature physeal closure.9 Acute suppurative intertrabecular osteomyelitis in the primary spongiosa of the metaphyses can lead to bone necrosis, failure of osseous tissue deposition onto the calcified cartilage lattice, trabecular microfractures, and defective bone formation.2 These abnormalities can lead to metaphyseal infarction and separation of the epiphysis. Elongation of the calcified-cartilage lattice of the primary spongiosa and impacted trabeculae can result in formation of a dense band adjacent to the growth plate.2,7,10 Subperiosteal hemorrhage and inflammation can also be seen.9 These pathological changes from the normal physeal development may result in permanent skeletal deformity of long bones.8 Spontaneous remission of clinical signs is common, and not all puppies experience multiple relapses.5 Relapses do not occur after long bones cease to grow, but diaphyseal deformities may persist.5 Corrective osteotomy may, on rare occasions, be required to correct such deformities.
The veterinary literature includes numerous reports of hypertrophic osteodystrophy occurring in the distal radius, ulna, and tibia.1–3,8,9 To the authors’ knowledge, no instance of hypertrophic osteodystrophy occurring in the proximal humerus has been reported. The purpose of this report is to describe hypertrophic osteodystrophy involving the proximal humerus in two young, male dogs.
Case Reports
Case No. 1
An approximately 6-month-old, 19.3-kg, intact male, mixed-breed dog was evaluated for nonweight-bearing lameness of both forelimbs. The owner reported an intermittent, mild to moderate lameness that had lasted >3 weeks. The referring veterinarian had initially taken survey radiographs and made comments to the owner suggestive of osteochondrosis of the left humerus. A 1-week course of carprofena (2.2 mg/kg per os [PO] q 12 hours), acepromazineb (1 mg/kg PO q 12 to 24 hours) for keeping the dog calm, and cage rest was prescribed; no improvement was seen.
On examination at the veterinary teaching hospital, the dog was laterally recumbent and depressed and had a rectal temperature of 40°C (104°F). Body condition score was acceptable. Diffuse, nonpitting, soft-tissue swelling was evident in both carpi. Signs of severe pain were elicited on palpation, flexion, and extension of both carpi and the left shoulder. The dog displayed generalized hyperesthesia during the physical examination. Results of a complete blood cell count (CBC) showed a mild monocytosis (1092/μL, reference range 0 to 840/μL). Serum biochemical abnormalities included hypoalbuminemia (1.7 g/dL, reference range 2.7 to 4.4 g/dL), low blood urea nitrogen (5 mg/dL, reference range 6 to 25 mg/dL), hyponatremia (121 mEq/L, reference range 139 to 154 mEq/L), hyperglobulinemia (5.7 g/dL, reference range 1.6 to 3.6 g/dL), and hyperphosphatemia (7.9 mg/dL, reference range 2.5 to 6 mg/dL). Results of a urinalysis revealed mild hematuria (1+).
Radiographs of both the right and left carpi and shoulders revealed an irregular radiolucent zone parallel to the physes of the distal radial, distal ulnar, and proximal humeral metaphyses [Figures 1, 2]. Areas of increased opacity within the metaphyses were between and parallel to the physes and the lucent zones.
The dog was admitted to the veterinary teaching hospital. Intravenous fluids were administered for approximately 24 hours to maintain hydration, and hydromorphonec (0.1 mg/kg intramuscularly [IM] q 6 hours) was administered to control pain. The following day, the dog was more comfortable and was discharged with a 1-week course of tramadold (4 mg/kg PO q 12 hours) and carprofen (2.2 mg/kg PO q 12 hours). The dog recovered well and resumed normal activity within a week. A follow-up telephone conversation 6 months later revealed the dog was healthy and free of clinical signs of hypertrophic osteodystrophy.
Case No. 2
A 3-month-old, 12.3-kg, intact male golden retriever was presented to the referring veterinarian because of an inability to stand. Physical examination revealed pain when the carpal and stifle joints were palpated. The puppy had a temperature of 39.7°C (103.4°F). Results of a modified CBC revealed a low hematocrit (26.2%, reference range 37% to 55%) and hemoglobin (9.2 g/dL, reference range 12 to 18 g/dL). Survey radiographs made by the referring veterinarian were suggestive of hypertrophic osteodystrophy of the distal radius, ulna, and tibia. Carprofen (2.2 mg/kg PO q 12 hours) was administered for 1 week, but no improvement was seen.
On presentation to the veterinary teaching hospital, the puppy was bright and alert but unwilling to stand. Slight pain was elicited on palpation of the right shoulder during the physical examination. Results of a CBC showed a lymphocytosis (5265 cells/μL, reference range 690 to 4500/μL) and thrombocytosis (497 × 103 cells/μL, reference range 170 to 400 × 103/μL). Serum biochemical abnormalities included a decreased alanine aminotransferase concentration (10 U/L, reference range 12 to 118 U/L), an elevated alkaline phosphatase concentration (186 U/L, reference range 5 to 131 U/L), hypercholesterolemia (685 mg/dL, reference range 92 to 324 mg/dL), and hyperphosphatemia (7.5 mg/dL, reference range 2.5 to 6 mg/dL).
Radiographs of the right and left carpi illustrated the previously described changes typical of hypertrophic osteodystrophy [Figures 3A, 3B]. Radiographic changes observed in the lateral projection of the right shoulder were also compatible with hypertrophic osteodystrophy. Irregular lucent zones were seen in the metaphysis of the proximal humerus adjacent to the physis [Figure 4]. Periosteal new bone proliferation was also seen caudomedial to the proximal metaphysis of the humerus that was separate from the cortex of the bone. A small amount of soft-tissue swelling was associated with the shoulder joint.
The puppy was discharged with instructions for carprofen (2.2 mg/kg PO q 12 hours) and tramadol (4 mg/kg PO q 12 hours) to be administered for 1 week. When contacted 3 months later, the owner reported that the dog’s activity level and behavior had returned to normal within 1 week after treatment of hypertrophic osteodystrophy and that no subsequent medical problems had developed.
Discussion
The diagnosis of hypertrophic osteodystrophy is usually straightforward and based on signalment, clinical signs, and radiographic findings. Careful examination and palpation of the long bones of a lame, skeletally immature dog reveals pain in the metaphyseal regions of the long bones.3 The two dogs in this report were presented for nonweight-bearing lameness, and pain was elicited when the shoulders were digitally palpated, flexed, and extended. Several developmental conditions of growing dogs can result in similar signs of shoulder pain, including osteochondritis dessicans, incomplete ossification of the caudal glenoid, glenoid dysplasia, and panosteitis. Although hypertrophic osteodystrophy appears to be a very uncommon cause of shoulder pain, it still should be considered as a differential diagnosis.
Classic hypertrophic osteodystrophy radiographic changes are typically found in the radius, ulna, and tibia.1–3,8,9 These changes include transversely oriented lucent zones within the metaphysis that are parallel and adjacent to the physis; this appearance is sometimes referred to as the “double physis” sign.9 Radiographs in both of these cases demonstrated the pathognomonic changes associated with hypertrophic osteodystrophy in the proximal humerus, as well as in the radius and ulna. A lateral radiographic view of the left shoulder in both cases showed an irregular radiolucent zone in the metaphysis of the proximal humerus adjacent to the physis. Some additional lucent zones appeared sclerotic on the proximal humerus in the 3-month-old puppy (case no. 2). In any young dog suspected of having hypertrophic osteodystrophy, the affected bone should be radiographed for evaluation.8
No specific treatment exists for hypertrophic osteodystrophy. Supportive treatment depends on severity of the clinical signs. Mildly affected dogs may need only mild analgesic therapy in the form of nonsteroidal antiinflammatory drugs (NSAIDs).3–5,7,8,10 More severely affected puppies often refuse to eat and stand. They may require opioids, intravenous fluids, nutritional assistance, and general nursing care.3,5,8,10 Corticosteroids should be avoided or used sparingly to avoid physeal growth disturbances. In these two cases, treatment with carprofen (2.2 mg/kg) and tramadol (4 mg/kg) resulted in an excellent response. One dog improved with some intravenous fluid therapy to maintain hydration.
In general, the prognosis for recovery from hypertrophic osteodystrophy is good. The severity of clinical signs can vary from mild lameness to moribund recumbency. Spontaneous remission of clinical signs is common, and not all puppies experience multiple relapses.5 Relapses do not occur after long bones cease to grow, but diaphyseal deformities may persist and become incompatible with a good quality of life.5
Conclusion
Hypertrophic osteodystrophy of the proximal humerus was diagnosed in two young, male dogs based on clinical signs and radiographic findings. Oral treatment with carprofen and tramadol successfully alleviated pain in both dogs. Hypertrophic osteodystrophy should not be overlooked as a possible diagnosis for shoulder pain in growing medium-, large-, and toy-breed dogs.
Rimadyl; Pfizer, Exton, PA 19341
Acepromazine; Boehringer Ingelheim, St. Joseph, MO 64506
Hydromorphone; Baxter, Deerfield, IL 60015
Tramadol; Corepharma, Middlesex, NJ 08846
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440342
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440342
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440342
Citation: Journal of the American Animal Hospital Association 44, 6; 10.5326/0440342
(Case no. 1): Craniocaudal radiographic views of the right and left antebrachium of a 6-month-old, intact male, mixed-breed dog presented for nonweight-bearing lameness of 3 weeks’ duration. Note the pseudophyseal line just proximal to the normal physis of the radius and ulna—a feature pathognomonic for hypertrophic osteodystrophy, more prominent in the left. (L=left antebrachium)
(Case no. 2): Craniocaudal radiographic projections of the right (A) and left (B) carpi of a 3-month-old, intact male golden retriever puppy that was presented for inability to stand. Note the “double physeal line” parallel to the physis of the distal radius and ulna, indicative of hypertrophic osteodystrophy.
(Case no. 2): Lateral radiographic view of the left shoulder of the same dog in Figure 3. Note irregular radiolucent zones in the metaphysis of the proximal humerus adjacent to the physis, the sclerotic appearance of the area surrounding these lucent zones, and bony proliferation in the caudal distal region of the humerus.
