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1
University Cambridge,
Cambridge, UK
2
Queen Mother Hospital for
Animals, Royal Veterinary
College, Hatfield, Hertfordshire,
UK
Correspondence to
Myfanwy Hill,
MYHILL@RVC.AC.UK
Received 3 November 2014
Revised 1 January 2015
Accepted 12 January 2015
To cite: Hill M, Scudder CJ,
Glanemann B, et al. Vet Rec
Case Rep Published online:
[please include Day Month
Year] doi:10.1136/vetreccr-
2014-000155
Hill M, et al. Vet Rec Case Rep 2015;3:e000155. doi:10.1136/vetreccr-2014-000155
COMPANION OR PET ANIMALS
Hypertrophic osteodystrophy in a dog imaged
with CT
Myfanwy Hill,1 Christopher J Scudder,2 Barbara Glanemann,2 Randi Drees2
SUMMARY
A seven-month-old male neutered cross-breed dog
presented with non-specific signs of lethargy, pyrexia
and pain on manipulation of the limbs, which
progressed over a period of 24 hours to a non-
ambulatory state with pain over multiple metaphyses.
The patient underwent diagnostic imaging examinations,
including radiography and CT, and arthrocentesis was
performed, which demonstrated a sterile, neutrophilic
infiltrate. On the basis of diagnostic tests, a diagnosis of
hypertrophic osteodystrophy was made. The patient was
managed initially with non-steroidal anti-inflammatory
medication and adjunctive analgesia. The patient failed to
respond to this protocol and hence was changed onto a
tapering course of steroids initially at immunosuppressive
levels to which he responded well. This case report
provides the first description of hypertrophic
osteodystrophy using CT and supports the use of
arthrocentesis in the diagnostic plan for suspected cases
of hypertrophic osteodystrophy in the dog.
BACKGROUND
This study details the first report of the radio-
graphic findings of CT features of hypertrophic
osteodystrophy (HOD), also known as metaphyseal
osteopathy, in a dog. Additionally, we report the
arthrocentesis findings of a sterile neutrophilic infil-
trate for this patient, which is little reported in the
literature.
CASE PRESENTATION
A seven-month-old, 15 kg, male entire, standard
poodle cross flat coat retriever presented for examin-
ation following a 24-hour history of stiffness when
walking and low head carriage. On examination he
was bright, alert and responsive, ambulatory, neuro-
logically appropriate and cardiovascularly stable.
The dog had a rectal temperature of 39.4°C.
General physical examination was otherwise unre-
markable. The dog was vaccinated, treated for fleas
and endoparasites, and received a commercially pre-
pared food with mince supplements.
Orthopaedic examination did not detect any
joint effusion, and pain could not be elicited on
manipulation of any joint of the axial or the appen-
dicular skeleton. Neurological examination was
normal.
The dog was initially treated with 3 mg/kg of tra-
madol orally every eight hours; however, he dete-
riorated over the following 24 hours, becoming
non-ambulatory and acutely painful on manipula-
tion of the thoracic limbs over the scapulohumeral
and carpal joints bilaterally, and over the proximal
Veterinary Record Case Reports
metaphyses of humerus and the distal metaphyseal
region of the antebrachium. Moderate bilateral
carpal joint effusion was present at this time.
INVESTIGATION
Serum biochemical analysis revealed serum total
protein concentration of 62 g/l, mild hypoalbuminae-
mia (26.9 g/l, Reference Interval (RI) 28.0–39.0), bor-
derline hyperphosphataemia (2.05 mmol/l, RI 0.80–
2.00) and mild hypercholesterolaemia (9.5 mmol/l,
RI 3.3–8.9). Moderate mature neutrophilia (23.7×
109/l, RI 3.0–11.5), mild monocytosis (2.80×109/l,
RI 0.15–1.50) with a packed cell volume of 40 per
cent was seen on complete blood cell count analysis.
Urinalysis obtained via cystocentesis had a urine spe-
cific gravity of 1.031, dipstick analysis was unremark-
able and no microorganisms were cultured.
At this stage, diagnostic testing and investigations
were focused at refining the list of possible differen-
tial diagnoses, which included immune-mediated
polyarthritis, septic arthritis, HOD, a septic focus
(pyrexia of unknown origin) or panostitis.
Survey radiographs of the thorax and abdomen
were unremarkable. In order to efficiently evaluate
the patient and obtain multiple joint studies, along-
side more detailed examination of the thorax and
abdomen, a CT examination (Philips Mx8000IDT,
Best, The Netherlands) of the thorax, abdomen
and forelimbs was performed under general anaes-
thesia using a high-frequency reconstruction algo-
rithm at 0.7 mm reconstructed slice thickness for
the forelimbs and medium ( preadministration and
postadministration of 800 mg I/mg intravenously)
and high-frequency reconstruction algorithm at
3 mm reconstructed slice thickness for the thorax
and abdomen (Fig 1).
CT examination showed moth-eaten lysis of the
proximal humeral and distal radial and ulnar meta-
physis with interspaced slightly increased bone
attenuation, bilaterally (Fig 2). Changes were
overall fairly symmetric, but the left proximal
humeral physis was affected most severely. The
epiphyses of the affected bones were normal, and
the physes were regionally minimally widened but
mostly considered normal. There was increased soft
tissue attenuation surrounding the affected regions,
and a mildly increased amount of synovial volume
was best seen in both shoulder joints. The axillary
and prescapular lymph nodes were bilaterally sub-
jectively enlarged, both measuring 0.7 W×2.5
W×2.7 L cm and 2.3 W×1.2 H×2.3 L cm. No
other lymph nodes were considered enlarged.
Based on these findings, HOD affecting the prox-
imal humeral, distal radial and ulnar metaphysis
1
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Veterinary Record Case Reports

FIG 1: Dorsal plane reconstruction of both shoulders (A) and oblique transverse plane reconstruction of the right shoulder (B) showing the
moth-eaten lysis (black arrows) along the proximal humeral physis interspaced with areas of hyperattenuating bone. The left side was slightly
more affected than the left. High-frequency reconstruction algorithm, 0.7 mm slice reconstruction thickness

was diagnosed, with additional mild swelling/effusion surround-
ing the affected sites.
Following CT examination, arthrocentesis of the effused
carpal joints was performed. Cytological evaluation of the fluid
showed a low to mildly increased cellularity with 43 per cent
non-degenerate population of neutrophils, 32 per cent mono-
cytes, 20 per cent macrophages and 5 per cent lymphocytes. No
microorganisms were visible, and bacterial culture was negative.
DIFFERENTIAL DIAGNOSIS
This patient was being evaluated for pyrexia of unknown origin
with primary differential diagnoses being HOD and immune-
mediated polyarthritis.
TREATMENT
The dog was started on a course of oral meloxicam at 0.2 mg/kg
on day 1, followed by 0.1 mg/kg on two subsequent days, and a
ketamine constant rate infusion (CRI) at 0.4 mg/kg/hour, and
methadone every four hours at 0.1–0.3 mg/kg to effect. After
three days, the dog had made no significant improvement and
hence it was decided to switch to an immunosuppressive course
of prednisolone. The ketamine CRI was stopped due to the
development of nausea. A 36-hour washout period was started
prior to prednisolone therapy, and omeprazole 1 mg/kg every
24 hours was initiated. Over this period, the nausea resolved.
Prednisolone at 2 mg/kg was given for 10 days before reducing
the dose to 1 mg/kg. Over this period, the analgesia was further
phased down; methadone was replaced with 3.3 mg/kg tramadol
orally every eight hours and 10 mg/kg paracetamol intraven-
ously every 24 hours.
The dog markedly improved and was discharged 10 days after
initial hospitalisation (day 5 of prednisolone therapy) on a taper-
ing course of prednisolone: 50 per cent reduction after the
initial 10 days (1 mg/kg), and then to 1.67 mg every other day
(based on approximately 1.5 mg/kg every other day) for
14 days, followed by a 25 per cent reduction in dose every
14 days thereafter.
OUTCOME AND FOLLOW-UP
At re-examination one week after discharge, the dog was ambu-
latory and had a normal physical examination. Orthopaedic
examination demonstrated pain only on manipulation of the left
shoulder, with manipulation of the right shoulder and both
carpal joints being well tolerated. Re-examination at one month

FIG 2: Dorsal (A) and transverse (B) plane reconstruction showing the lytic changes (black arrows) in the distal radial physes consistent with
hypertrophic osteopathy. Note that the moth-eaten pattern is best seen in the transverse plane reconstruction. Additional soft tissue swelling
can be seen primarily surrounding the right perilesional region (white arrows). High-frequency reconstruction algorithm, 0.7 mm slice reconstruction
thickness

2 Hill M, et al. Vet Rec Case Rep 2015;3:e000155. doi:10.1136/vetreccr-2014-000155

 Downloaded from http://vetrecordcasereports.bmj.com/ on July 13, 2015 - Published by group.bmj.com
after discharge found the dog to have a normal general physical
and orthopaedic examination and unremarkable serum bio-
chemical and haematological values.
DISCUSSION
HOD, although uncommon, typically affects young growing
large and giant breed dogs (LaFond and others 2002). The
disease is also known as canine metaphyseal osteopathy and has
an unknown pathogenesis, which is likely to be multifactorial
(Schulz and others 1991, Munjar and others 1998, Harrus and
others 2002). Many underlying aetiologies have been suggested,
including vaccine associations, nutritional deficiencies, microor-
ganisms and genetic predispositions (Munjar and others 1998,
LaFond and others 2002).
HOD has been identified in 40 breeds of dog (Munjar and
others 1998), with most breeds represented sporadically within
the veterinary literature. The disease has affected entire litters of
Weimaraner puppies (Abeles and others 1999) with clinical
signs typically developing at three to four months of age,
though they have been observed as early as two months of age
and as late as the time of physeal closure (Muhlbauer and
Kneller 2013). Male dogs are at 2.3 times greater risk of develop-
ing the condition than female dogs, and the Great Dane is over-
represented in the reported population (Munjar and others 1998).
The most common presenting complaints include gait abnor-
malities, pyrexia and pain on joint manipulation (Abeles and
others 1999, Joiner and Montgomery 2011, Safra and others
2013). In addition, anorexia, vomiting, diarrhoea, weight loss,
respiratory signs and nasal discharge have been reported (Abeles
and others 1999, Safra and others 2013).
Serum biochemical and haematological abnormalities previ-
ously reported include serum changes consistent with juvenile
life stage; hyperphosphataemia and elevated alkaline phosphat-
ase activity, and other non-specific changes including reduced
urea and creatinine levels, have been reported. Non-specific
haematological abnormalities including mild non-regenerative
anaemia, leucocytosis, thrombocytosis and thrombocytopaenia
have also been reported (Abeles and others 1999, Harrus and
others 2002, Safra and others 2013).
Joint fluid analysis has been reported in two other case
reports (Woodard 1982, Arnott and others 2008); in both cases,
a sterile polymorphonuclear neutrophilic infiltrate was
identified.
Radiographic appearance of lesions is typically of a periosteal
hyperplasia and calcification (Carbery and Thompson 1976),
creating a ‘moth-eaten’ appearance. Lesions are usually symmet-
ric and may occur on any long bone metaphysis; however, other
locations have been reported, including the mandible, cranium
and ribs. A line of reduced opacity adjacent to the physis can be
seen as the predominant finding; this has been described as a
double physeal sign. The physis itself appears normal, and mild
metaphyseal flaring may be present. Swelling of the soft tissues
is not uncommon. Later in the disease boney cuffs may develop
along the metaphysis and periosteal reaction can be seen
(Olsson 1972, Muhlbauer and Kneller 2013).
Treatment is non-specific and is aimed at managing the
pyrexia and the bone pain using either non-steroidal medication
or steroids with adjunctive analgesia as necessary (Abeles and
others 1999, Miller 2001, Safra and others 2013).
Relapses of the disease are possible and should be treated
using the regimen that was most effective for the preceding
event (Abeles and others 1999, Safra and others 2013). Relapses
may occur up until the closure of the growth plates has com-
pleted, and dogs with severe disease may develop angular limb
Hill M, et al. Vet Rec Case Rep 2015;3:e000155. doi:10.1136/vetreccr-2014-000155
Veterinary Record Case Reports
deformity or even pathological fracture secondary to disease
(Demko and McLaughlin 2005).
In the case reported here, the joint effusion was similar in
nature to those seen in immune-mediated polyarthritis, which is
consistent with the two previous case reports. However, in the
first of these cases, chloramphenicol was administered prior to
treatment (Woodard 1982), and in the second case, pathological
fractures were identified, which is an atypical finding for the
disease process (Arnott and others 2008). Arthrocentesis may,
therefore, be indicated as an additional diagnostic tool, and
further reports of the character of the synovial fluid may allow
further critical analysis of the natural history of the disease.
Diagnosis of HOD is frequently made on conventional radio-
graphs; this patient underwent diagnostic imaging using CT as
immune-mediated polyarthropathy was considered a differential
diagnosis. Therefore, CT examination would allow ruling out
further underlying causes and determine the extent of disease.
Investigation of cases where polyarthritis is a differential diagno-
sis includes the differentiation of erosive and non-erosive forms
of polyarthritis (Bennett 1987a,b,c,d), as well as determining
whether the disease processes are primary or secondary.
Secondary diseases are considered to be graded I to IV (Bennett
and Kelly 1987), and bicavity imaging is recommended in order
to accurately categorise the condition. The cross-sectional exam-
ination in this case elegantly demonstrated the metaphyseal
changes in the affected bones also enabled the demonstration of
the associated changes, including joint effusion, perilesional soft
tissue swelling and regional lymphadenopathy. Disease primarily
affecting the physes or joints or any thoracic or abdominal
disease was effectively ruled out using CT.
To our knowledge, CT findings of HOD have not been previ-
ously reported in dogs. Musculoskeletal CT examinations cur-
rently find most application for orthopaedic diseases in
veterinary patients. CT examination of the long bones has been
primarily used in diagnosing neoplastic bone disease (Davis and
others 2002, Vanel and others 2002, Karnik and others 2012)
and allows for very specific determination of tumour margins
based on its cross-sectional nature. There has been limited use
of this modality for diagnosis of musculoskeletal diseases in the
growing canine patient, but the cross-sectional nature and high
resolution of bony structures lend itself favourably to the careful
evaluation of the epiphyseal, physeal and metaphyseal struc-
tures, and 3D modelling allows further understanding of pos-
sible present limb deformities (Dismukes and others 2008,
Meola and others 2008). Additionally, CT examination of the
appendicular skeleton can be conducted concurrently with
bicavity imaging, facilitating a more streamlined diagnostic plan.
This report suggests that this is a useful modality that may offer
the potential for early diagnosis of this condition as it may
allow for identification of more subtle bony changes than stand-
ard radiography. Ideally CT could also be used to follow up on
bone healing but was not applied in this case as no complica-
tions were encountered. However, conventional radiographs
will remain an inherent component of the work of these cases
in most first opinion practices.
Clearly it would be ill advised to embark upon a treatment
protocol that included both steroids and non-steroidal anti-
inflammatories (Whitely and Day 2011). It would therefore be
useful to the clinician to have additional tools that might allow
differentiation between those patients who are likely to respond
to non-steroidal anti-inflammatory medication and those who
may not. Arthrocentesis may be of utility in this regard;
however, further data are required to establish the diagnostic
evaluation of this disease.
3
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Veterinary Record Case Reports

Contributors All authors contributed to the production of the manuscript. MH was
the primary author with CJS, BA and RD contributing equally. Images were prepared
by RD.
Competing interests None.
Provenance and peer review Not commissioned; externally peer reviewed.
REFERENCES
ABELES V., HARRUS S., ANGLES J. M., SHALEV G., AIZENBERG I., PERES Y., AROCH I.
(1999) Hypertrophic osteodystrophy in six Weimaraner puppies associated with systemic
signs. Veterinary Record 145, 130–134
ARNOTT J. L., PHILBEY A. W., BENNETT D. (2008) Pathological fractures secondary to
metaphyseal osteopathy in a dog. Veterinary and Comparative Orthopaedics and
Traumatology 2, 177–180
BENNETT D. (1987a) Immune-based erosive inflammatory joint disease of the dog.
Canine Rheumatoid Arthritis. II. Pathological investigations. Journal of Small Animal
Practice 28, 799–819
BENNETT D. (1987b) Immune-based erosive inflammatory joint disease of the dog.
Canine Rheumatoid Arthritis. I. Clinical, radiological, and laboratory investigations.
Journal of Small Animal Practice 28, 779–797
BENNETT D. (1987c) Immune-based non-erosive inflammatory joint disease of the
dog. I. Systemic Lupus erythematosus. Journal of Small Animal Practice 28, 871–889
BENNETT D. (1987d) Immune-based non-erosive inflammatory joint disease of the dog.
III. Canine idiopathic polyarthritis. Journal of Small Animal Practice 28, 909–928
BENNETT D., KELLY D. F. (1987) Immune-based non-erosive inflammatory joint disease of
the dog. II. Polyarthritis/polymyositis syndrome. Journal of Small Animal Practice
28, 891–908
CARBERY J. T., THOMPSON K. S. (1976) Hypertrophic osteodystrophy in a cattle dog.
New Zealand Veterinary Journal 24, 267
DAVIS G. J., KAPATKIN A. S., CRAIG L. E., HEINS G. S., WORTMAN J. A. (2002)
Comparison of radiography, computed tomography, and magnetic resonance imaging
for evaluation of appendicular osteosarcoma in dogs. Journal of the American
Veterinary Medical Association 220, 1171–1176
DEMKO J., MCLAUGHLIN R. (2005) Developmental disease of the dog. Veterinary Clinics
of North America: Small Animal Practice 35, 1111–1135
DISMUKES D. I., FOX D. B., TOMLINSON J. L., ESSMAN S. C. (2008) Use of radiographic
measures and three-dimensional computed tomographic imaging in surgical correction
of an antebrachial deformity in a dog. Journal of the American Veterinary Medical
Association 232, 68–73
HARRUS S., WANER T., AIZENBERG I., SAFRA N., MOSENCO A., RADOSHITSKY M.,
BARK H. (2002) Development of hypertrophic osteodystrophy and antibody response in
a litter of vaccinated Weimaraner puppies. Journal of Small Animal Practice 43, 27–31
JOINER K. S., MONTGOMERY R. D. (2011) Pathology in Practice: Veterinary Medicine
today. Journal of the American Veterinary Medical Association 238, 1413–1415
KARNIK K. S., SAMII V. F., WEISBRODE S. E., LONDON C. A., GREEN E. M. (2012)
Accuracy of computed tomography in determining lesion size in canine appendicular
osteosarcoma. Veterinary Radiology & Ultrasound 53, 273–279
LAFOND E., BREUR G. J., AUSTIN C. C. (2002) Breed susceptibility for developmental
orthopedic diseases in dogs. Journal of the American Animal Hospital Association
38, 467–477
MEOLA S. D., WHEELER J. L., RIST C. L. (2008) Validation of a technique to assess radial
torsion in the presence of procurvatum and valgus deformity using computed
tomography: a cadaveric study. Veterinary Surgery 37:525–529
MILLER C. (2001) Hypertrophic osteodystrophy in a great Dane Puppy. The Canadian
Veterinary Journal 42, 63–66
MUHLBAUER MC, KNELLER SK. (2013) Radiography of the Dog and Cat: guide to
making and interpreting radiographs. Wiley-Blackwell. p 185.
MUNJAR T. A., AUSTIN D. D., BREUR G. J. (1998) Comparison of risk factors for
hypertrophic osteodystrophy, craniomandibular osteopathy and canine distemper virus
infection. Veterinary and Comparative Orthopaedics and Traumatology 11, 37–43
OLSSON S. E. (1972) Radiology in veterinary Pathology. A review with special reference to
hypertrophic osteodystrophy and secondary hyperparathyroidism. Acta radiologica.
Supplementum 319, 255–270
SAFRA N., JOHNSON E. G., LIT L., FOREMAN O., WOLF Z. T., AGUILAR M., KARMI N.,
FINNO C. J., BANNASCH D. (2013) Clinical manifestations, response to treatment and
clinical outcomes for Weimaraners with Hypertrophic Osteodystrophy: 53 cases
(2009–2011). Journal of the American Veterinary Medical Association 242,
1260–1266
SCHULZ K. S., PAYNE J. T., ARONSON E. (1991) Escherichia coli bacteremia associated
with hypertrophic osteodystrophy in a dog. Journal of the American Veterinary Medical
Association 199, 1170–1173
VANEL M., BLOND L., VANEL D. (2002) Imaging of primary bone tumors in veterinary
medicine: which differences? European Journal of Radiology 82, 2129–2139
WHITELY N. T., DAY M. J. (2011) Immunomodulatory drugs and their application to the
management of canine immune mediate disease. Journal of Small Animal Practice
52, 70–85
WOODARD J. C. (1982) Canine hypertrophic osteodystrophy, a study of spontaneous
disease in littermates. Veterinary Pathology 19, 337–354

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4 Hill M, et al. Vet Rec Case Rep 2015;3:e000155. doi:10.1136/vetreccr-2014-000155

 Downloaded from http://vetrecordcasereports.bmj.com/ on July 13, 2015 - Published by group.bmj.com

Hypertrophic osteodystrophy in a dog

imaged with CT
Myfanwy Hill, Christopher J Scudder, Barbara Glanemann and Randi
Drees

Vet Rec Case Rep 2015 3:

doi: 10.1136/vetreccr-2014-000155

Updated information and services can be found at:

http://vetrecordcasereports.bmj.com/content/3/1/e000155

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References This article cites 24 articles, 3 of which you can access for free at:
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Topic Articles on similar topics can be found in the following collections

Collections Companion or pet animals (98)
Companion or pet animals: Dogs (65)
Imaging (37)
Internal medicine (19)
Orthopaedics (10)

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