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An Unusual Case of Diaphyseal Osteomyelitis
Ashoo Agarwal*, Sandeep Dhote**, A Govindan***, S Vijay+, V Shanmugam+, M Paul Korath#, K Jagadeesan##

Diaphyseal location and association with blunt trauma makes this presentation of osteomyelitis quite challenging for a treating surgeon and histopathology is the key to correct diagnosis.
This case is perhaps one more shade in the spectra of presentation of osteomyelitis.

The term osteomyelitis was introduced by Nelaton in 1844 and implies an inflammation of the bone caused by an infecting organism.1,2 The infection may be limited to a single portion of the bone or may involve a number of regions such as the marrow, cortex, periosteum, and even the surrounding soft tissue.2

We report an unusual case of subacute diaphyseal osteomyelitis of left tibia in an adult male. The case is presented for its unusual clinical and radiographic features with respect to its site and presentation.

Case Report
A thirty-eight year old male presented with history of accidental blunt injury to the front of his left lower leg about two and a half months back. There was history of pain in his left lower leg since then, on walking. There was no history of an open wound on the leg following the injury. There was no history of fever.
On examination the patient was well built, had normal vital signs and mild pedal oedema in the left leg. He had mild tenderness over the mid portion of left lower leg, anteriorly, with minimal swelling. The skin over the swelling was otherwise normal and there was no adherence of the skin to the bone. There was no distal neurovascular deficit in the left leg.

The basic preliminary blood investigations were in the normal range. Anteroposterior and lateral radiographic films of left lower leg showed a fairly well defined, solitary lytic lesion of approximate size 3 x 2 cms, without sclerotic margins and sharp transition to normal bone, in the medullary portion of the mid-shaft of tibia, with no evidence of periosteal reaction. A three phase whole body scan with TC-99M-MDP (methylene diphosphonate) showed increase in uptake of tracer both in the blood-pool phase reflecting increased blood flow and in the delayed scan reflecting increase in bone turnover and osteomyelitis was strongly suspected. Axial computerized tomography scan of both the lower legs showed irregular expansion of medullary cavity with cortical thinning, and cortical breach on the anteromedial surface of mid shaft of left tibia.

Fig. 1 : Antero-posterior and lateral radiograph of left lower leg showing a well defined solitary lytic lesion of approximately 3 x 2 cm in the medulla of the midshaft of tibia with a narrow zone of transition. Neither sclerosis of the margin nor any periosteal reaction seen.

Fig. 2 : 99mTc - methylene diphosphonate (MDP) radionuclide whole body bone scan shows increased uptake in the lesion on delayed phase. (Increased uptake was also noted on the blood pool phase)

Fig. 3 : Non contrast axial CT scan of both the lower extremities showing irregular expansion of the medullary cavity of the left tibia in the midshaft with cortical thinning and breach on the antero-medial surface.

Subsequently the patient underwent open biopsy of the lesion under spinal anaesthesia. Thereafter the patient was managed conservatively with antibiotics and anti-inflammatory drugs. Histopathological examination of the post-operative specimen showed necrotic bony spicules, florid granulation tissue and sheets of foamy macrophages suggestive of osteomyelitis. The wound swab on culture grew staphylococcus epidermidis and streptococcus viridans.
The patient was responding well to the treatment given.

Osteomyelitis can be classified on the basis of a number of criteria such as the duration of infection (acute, subacute, or chronic); its mechanism (exogenous or haematogenous); and the type of host response to the infection (pyogenic or nonpyogenic).2

The most common source of osteomyelitis in skeletally immature patients is haematogenous. Because of differences in vascular anatomy in infants, children, and adults, the pathologic and radiologic features of infection differ in these age groups. In infants, involvement of metaphysis with epiphyseal extension is common. In children, haematogenous spread is often localized in the metaphysis of long tubular bones. In adults, haematogenous osteomyelitis is rare in the extremities, but may be seen in the spine, pelvis, and small bones of hands and feet.1-4

Osteomyelitis in adults occurs more commonly by direct implantation or spread from a contiguous source of infection. The sites typically affected by contiguous spread of infection include the hands, feet, skull, mandible, and maxilla. Direct implantation of infection usually results from deep puncture wounds, animal bites, open fractures, or surgical procedures.

The clinical presentation in acute haematogenous osteomyelitis is often dramatic with sudden onset of high fever, a toxic state, and local signs of inflammation, although this presentation is not uniform.2 The patient may present with vague complaints such as local pain of long duration with minimal if any temperature elevation especially in case of adults.1

Compared with acute osteomyelitis, subacute osteomyelitis has a more insidious onset and lacks the severity of symptoms (as seen in our case). Temperature is only mildly elevated if at all. Pain of mild to moderate degree is one of the only consistent signs suggesting the diagnosis (as seen in our case). Laboratory evaluation is unrevealing, with a normal white blood cell count and differential. The erythrocyte sedimentation rate is elevated in only 50% of patients and blood cultures are negative (not done in our case). Plain roentgenograms and bone scans generally are positive, like in our case. Radiographs outline radiolucent areas with adjacent sclerosis and the lucent region is commonly located in the metaphysis.2 But in our case the lytic area seen was not surrounded by any sclerotic margins and was located in diaphysis.

The indolent course of subacute osteomyelitis is thought to be the result of increased host resistance, decreased bacterial virulence, or the administration of antibiotics before the onset of symptoms.2 In our case it was speculated that the combination of the organism of low virulence with a strong host response allowed the inflammation to persist in bone without producing significant signs or symptoms. The correct diagnosis is largely dependent on clinical suspicion and roentgenographic findings and must be established by an open biopsy and culture (as was done in our case). Staphylococcus aureus and Staphylococcus epidermidis (the one found in our case) are the predominant organisms identified in subacute osteomyelitis. The treatment of a culture positive infection includes surgical debridement and antibiotic therapy.2,3 In our case the patient was treated with surgical biopsy, debridement, adequate doses of oral antibiotics, anti-inflammatory drugs and he responded well.

Traditional teaching has always stressed, and correctly so, that the predominant site for the occurrence of osteomyelitis is the epimetaphysis of the long bones owing to the stagnation of the inflowing blood in this region of a bone. Our case is a subacute osteomyelitis in the diaphysis of the left tibia, histopathologically proved. We searched extensively in the English literature for similar reported cases of osteomyelitis in the diaphysis of long bones but were unable to find any. Similarly the association of osteomyelitis with blunt trauma could not be traced by us in our search of literature.


  1. Donald Resnick. Diagnosis of bone joint disorders. Fourth Edition, 2002; Chapter 59, Volume 3.
  2. Campbell’s operative orthopaedics. Tenth Edition, 2003; Chapter 16, Volume 1.
  3. Hayes CS, Heinrich SD, Craver R, et al. Subacute osteomyelitis. Orthopedics 1990; 13 (3) : 363-6.
  4. Jack S. Remington, Morton N Swartz. Current clinical topics in infectious diseases. Blackwell Science, 2002.


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*DNB Resident, **Head, Department of Radiodiagnosis; +Consultant Orthopaedician; #Chief Physician’ ##Chief Surgeon and Director; KJ Hospital Research and Postgraduate Centre, Chennai - 600 084.