Keywords
radioulnar ischaemic necrosis - osteonecrosis - haematogenous osteomyelitis - sequestrum
Introduction
Radioulnar ischaemic necrosis (RUIN) is a term that has been used to describe osteonecrosis
secondary to ischaemia of the radius and ulna in the dog.[1] There is a small amount of data in the literature describing the radiographic appearance
of a RUIN lesion.[1] Osteonecrosis in dogs has also been reported to occur with Legg-Calves-Perthes,
idiopathic osteonecrosis of the carpal bone and maxillofacial osteonecrosis.[2]
[3]
[4] This is the first case report of concurrent haematogenous osteomyelitis and ischaemic
necrosis occurring at the site of a lesion that is radiographically consistent with
RUIN.
History and Clinical Findings
An 11-month-old intact female Golden Retriever presented to the Veterinary Medical
Teaching Hospital of the University of California - Davis, School of Veterinary Medicine
for evaluation of a nontraumatic right thoracic limb lameness. The patient had a 3–4
week history of waxing and waning lameness that had been managed with a combination
of carprofen (3.9 mg/kg per os [PO] SID), tramadol (unknown dose) and cage rest. The
referring veterinarian suspected panosteitis due to the lack of overt radiographic
findings in the right thoracic limb. On examination, the dog was bright, with vital
parameters within normal limits, a body condition score of 4/9 and a weight of 25.5 kg.
The patient had a marked right thoracic limb lameness with decreased weight bearing
function, moderate ipsilateral muscle atrophy and subtle right carpal valgus. The
patient was painful during shoulder extension, and on long-bone palpation of the right
radius, right ulna and bilaterally along the femurs. The referring veterinarians'
radiographs were reviewed by a radiologist, deemed of good quality, and a definitive
cause for the lameness was not detected.
Imaging, Diagnosis and Outcome
A computed tomography (CT) scan revealed focal lysis of the proximal right radius
with a large thin sequestrum and marked endosteal and periosteal new bone formation
centred at the nutrient foramen ([Fig. 1]). The contralateral limb CT was within normal limits. The imaging characteristics
of the right thoracic limb were suggestive of osteomyelitis and additional diagnostics
were performed, including an ophthalmic fundic examination, haematology, chemistry
panel, urinalysis, urine culture and thoracic radiographs, all of which were unremarkable.
A fine-needle aspirate from the region adjacent to the right radial sequestrum in
the region of the involucrum had marked suppurative, septic inflammation featuring
rod-shaped bacteria. The sample was highly cellular and comprised mostly of neutrophils
that were often karyolitic with phagocytized rod-shaped bacteria and fewer variably
vacuolated macrophages. Aerobic, anaerobic and fungal cultures of the bone aspirate
were negative, which may be attributed to a low volume sample.
Fig. 1 Computed tomographic images of a sharp (bone) kernel of the right thoracic limb.
(A and B) Sagittal multiplanar reconstructions demonstrating a thin bone sequestrum along
the caudal radial cortex with smooth periosteal reaction along dorsal cortical margin
and extensive new endosteal new bone formation. (C) A transverse plane at the level of the sequestrum. (D) A dorsal plane of the sequestrum in the radius.
The patient was sent home on antibiotic medications (Clavamox; 14.7 mg/kg PO q12 × 14
days) with a recommendation for strict cage rest and continuation of carprofen (3.9 mg/kg
PO q24 as needed for pain). Re-evaluation with potential surgical removal of the sequestrum
was discussed.
On Day 24, the dog was improving clinically at home. Re-evaluation revealed she was
mildly lame on the right thoracic limb with mild, nonpainful swelling over her right
radius. Radiographs were acquired at this recheck evaluation and the osseous sequestrum
was not detected. A recheck sedated CT scan was performed for further investigation
and showed a healing lytic lesion of the radial diaphysis, and resolution of the sequestrum
([Fig. 2]). Since the dog was clinically improving and imaging showed a resolving lesion,
surgery was no longer indicated. Continued exercise restriction, antibiotic medication
and trazodone (5.8 mg/kg PO q12 as needed) were recommended.
Fig. 2 Computed tomographic images 24 days after presentation of the right thoracic limb.
(A and B) Sagittal multiplanar reconstructions at the level of the previous sequestrum. The
sequestrum is no longer visualized and a concave region of lysis persists in the caudal
radial cortex at the level of the nutrient foramen. (C) A transverse plane showing the concave lysis of the caudal radial cortex with severe
endosteal new bone and smooth periosteal reaction. (D) A dorsal plane of the caudal radial cortex.
On day 41, the dog had a recheck examination. She was no longer lame on physical examination,
and had no pain elicited on long bone palpation over the lesion previously identified
on her right radius and ulna. A CT was performed. The lesion had continued to resolve
with smooth margins, milder periosteal reaction and markedly reduced medullary sclerosis
([Fig. 3]). The patient was discharged and advised to resume physical activity since she was
clinically normal and the CT demonstrated improvement in the osteolytic lesion.
Fig. 3 Computed tomographic images 41 days after initial presentation of the right thoracic
limb shows great improvement in the lesion. (A and B) Sagittal multiplanar reconstructions, a concave divot persists in the caudal radial
cortex at the level of the nutrient foramen, the endosteal sclerosis has greatly improved.
(C) A transverse plane. (D) A dorsal multiplanar reconstruction.
Discussion
Bone sequestration is a radiographic and pathological finding more commonly described
in large animals than in small animals.[5]
[6] A bone sequestration is pathologically defined as a nonviable fragment of bone that
has lost its blood supply through a necrotic process. Radiographically, it manifests
as a sharply marginated sclerotic bone fragment surrounded by a radiolucent zone.
Bone sequestra can be sterile or infectious and can sometimes involve a draining tract.[7] In dogs, formation of sequestra is most often associated with osteomyelitis following
traumatic fractures and/or an orthopaedic surgical complication.[8]
[9]
[10]
[11]
[12]
In this instance, osteomyelitis was diagnosed based on the imaging features of an
aggressive bone lesion and the presence of septic suppurative inflammation in the
involucrum. Fine-needle aspirates are minimally invasive and have been successfully
used to diagnose bony lesions in both veterinary and human medicine.[2]
[13]
[14]
[15]
[16]
[17] Although histopathology from a surgical biopsy could have strengthened our diagnosis,
it was not performed due to the positive clinical response in the recheck interim
and the difficulty of reaching the lesion.
Osteomyelitis is an infection of the bone and marrow occurring from three main pathogeneses:
haematogenous, contiguous and direct inoculation.[18] In dogs, osteomyelitis most commonly occurs from direct inoculation of bacteria
and fungi from an open wound or after osteosynthesis; however, haematogenous spread
with seeding at the vascular metaphyses of long bones and near the nutrient foramen
has also been described.[19]
[20] The lack of a history of trauma and the location of the lesion centred at the nutrient
foramen of the radius in this case make haematogenous osteomyelitis most likely.
Osteonecrosis, ischaemic necrosis and avascular necrosis are all terms used to describe
the process of cell death caused by loss of blood supply to the bone.[21]
[22] Radioulnar ischaemic necrosis is defined as osteonecrosis of the radius and/or ulna
in the dog due to ischaemic injury of unknown aetiology.[1] Radiographically, RUIN lesions appear as osteolytic lesions on the opposing radial
and ulnar cortices. The caudal interosseous artery feeds the intramedullary blood
supply of both the radius and ulna. The radial nutrient foramen, which is typically
evident on lateral radiographs, lies along the caudal cortical margin approximately
1/3 the way down the diaphysis. The ulnar nutrient foramen is through the opposing
dorsal cortical margin just proximal to the radial nutrient foramen at about the level
where the radius and ulna become superimposed on a lateral radiograph.
This is also the region of the interosseous ligament, which spans the space between
the radius and ulna. The interosseous ligament has a wide insertion along the proximal
1/3 of the radius from the nutrient foramen proximally to a wider attachment along
the proximal 1/2 of the ulna. Frequently, there is enthesis new bone at the insertion
of the interosseous ligament creating an irregular margin to the opposing cortices.
This insertional desmopathy confounds interpretation of this region because it is
not uncommonly seen in dogs without lameness.[23] Concavities or lucencies have been described at the insertion of the interosseous
ligament varying in size from 2 to 10 mm.[24] The osseous changes seen with interosseous desmopathy are indicative of chronic
or previous change. While a definitive cause for the concavities at the insertion
of the interosseous ligament is unknown, one proposed hypothesis is previous desmopathy
of the interosseous ligament in a juvenile patient that altered normal radial widening
of the bone in this region while the adjacent bone grew normally. This hypothesis
presumes an alteration in the blood supply at the site of the interosseous insertion.[24]
The terminology of RUIN has been applied to describe these concave lucencies along
apposing margins of the radius and ulna regardless of the pathophysiology whether
these lesions may be a manifestation of chronic interosseous desmopathy or any cause
for ischaemia. In this case, the patient presented with a sequestrum, osteolysis with
marked endosteal and periosteal reaction centred at the nutrient foramen of the proximal
right radius. A haematogenous osteomyelitis was the primary differential given the
sequestrum, location and appearance. Cytology findings support a bacterial aetiology
with septic inflammation and rod-shaped bacteria. However, the location also fits
with a RUIN lesion, and on subsequent imaging studies the lesion had characteristics
similar to those described for a RUIN lesion with smoothly margined lysis of the caudal
radial cortex and adjacent smooth periosteal new bone formation.
Interestingly both RUIN lesions and sequestra form due to ischaemia of the bone, implying
that these lesions are not exclusive entities. This case appears to be an example
of RUIN in conjunction with osteomyelitis and subsequent bone sequestration. A transient
bacteraemia prior to presentation to XXX causing haematogenous osteomyelitis in the
radius and ulna is suspected given the nutrient foramen involvement. The inflammatory
response of the bone to a haematogenous infection could cause damage to the supplying
arteries disrupting the blood supply to the surrounding bone. Alternatively, a region
of ischaemia has a degree of immune privilege that can favour bacterial growth. Pathogenesis
of osteonecrosis and formation of a sequestrum have a lot of similarities supporting
the idea that they may occur simultaneously. Both are caused by disruption of blood
supply leading to cell necrosis. Radiographically, both involve a lucent region, the
only difference being that sequestra have a central piece of sclerotic bone within
the lucent rim. Thus, it makes sense to propose in this case that their pathogeneses
were linked.
The purpose of this case study was to present another case example of RUIN as there
is a paucity of published information in the literature. We postulated an aetiology
other than trauma and chronic desmopathy as a cause for RUIN lesions. In the present
case, there is evidence of an infectious aetiology, given the presence of a sequestrum,
the results of the fine-needle aspirate and the clinical response to antibiotic medications.
Whether the infection was a primary or a secondary remains unclear, but the lack of
corresponding soft tissue swelling and the close proximity of a nutrient foramen suggest
haematological seeding.
A larger case series or retrospective study of cases with correlated pathological
and clinical findings is needed to better understand the aetiology of RUIN and the
clinical impact it may have on dogs. This is complicated by the fact that many of
the patients that are diagnosed with RUIN lesions radiographically have no lameness;
there is great variability to the appearance of degenerative change at the insertion
of the interosseous ligament that may or may not have associated osteonecrosis and
as this case demonstrates these lesions can remodel and change over time.
