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Bone infarction

Dr Yuranga Weerakkody and Dr Andrew Dixon et al.

A bone infarction is a term used to refer to osteonecrosis within the metaphysis or diaphysis of a bone. A medullary infarct is a fairly equivalent term to bone infarct but is less frequently used. The term may also be applied to some cases involving the epiphysis, but should not be used to describe subchondral osteonecrosis, when avascular necrosis is preferred.

Pathology

Infarction begins when blood supply to a section of bone is interrupted. Once an infarct is established, a central necrotic core develops which is surrounded by a hyperaemic ischaemic zone. With time collagen granulation tissue becomes layered around the necrotic core. Demarcation between the normal surrounding marrow, the ischaemic zone and the necrotic core accounts for many of the radiographic appearances of bone infarcts.

Causes

General causes of osteonecrosis include

trauma
Caisson disease
haemoglobinopathies e.g. sickle cell disease ¹
radiotherapy
connective tissue disorders
renal transplantaion
corticosteroid excess (both endogenous and exogenous)
pancreatitis
gout
Gaucher's disease
alcohol

The above list applies to both bone infarct and subchondral avascular necrosis, however some conditions are more likely to lead to one over the other. Sickle cell disease and Gaucher's disease for instance very commonly cause bone infarcts and less commonly cause subchondral AVN.

Radiographic features

General features include

medullary lesion
serpiginous border
most common in metaphyses
often symmetrical / multiple infarcts

Plain film

There is significant delay between infarct onset and development of radiographic signs. Classic description is of medullary lesion of sheet-like central lucency surrounded by shell-like sclerosis with serpiginous border. Discreate calcification and perisotitis may also be seen.

CT

Generally does not reveal much more than the plain film.

MRI

An important feature in differentiating bone infarct from other medullary lesions is that the central signal usually remains that of normal marrow. The marrow is not replaced.

T1
- serpigionous peripheral low signal due to grannulation tissue and to lesser extent sclerosis
- peripheral rim may enhance post gadolinium
- central signal usually that of marrow
T2
- acute infarct may show ill-defined non-specific area of high signal
- double-line sign: hyperintense inner ring of granulation tissue and a hypointense outer ring of sclerosis
- absence of double-line sign does not exclude bone infarct
- central signal usually that of marrow
GE - gradient echo
- will also show double-line
- oedema obscured by susceptibility