AP view of left shoulder
AP view of left shoulder
Click an image for a more detailed view.
This case can be diagnosed on the single image presented above, but it is admittedly a bit difficult, due to the subtlety of the osteonecrosis. Once both of these findings have been noted, one has to put these two findings together to come up with the diagnosis of renal disease.
The humeral head flattening, though subtle, has a fairly short differential diagnosis: trauma or osteonecrosis. One can see impaction fractures involving the humeral head, but most of these seem to be associated with dislocations, such as the classic Hill-Sachs impaction seen with an anterior dislocation. However, the location of this patient's flattening is a bit atypical for a Hill-Sachs impaction fracture.
Though subtle, this impaction is more typical for that seen in osteonecrosis, due to collapse of the subchondral bone. Why does osteonecrotic bone collapse? This probably happens as a result of many cumulative microfractures, developed during the many travails and microtraumas of modern life. However, in normal living bone, these microfractures tend to heal relatively quickly, and enough of them never accumulate to the point of causing an actual macrofracture. Fracture healing does not occur in osteonecrotic, or dead bone. Therefore, these microfractures can accumulate for quite some time until the bone finally fails.
Osteonecrosis is a multifactorial process, and includes the following entities in its differential:
| Differential Diagnosis of Osteonecrosis | ||
| General cause | Specific cause | Pathophysiology |
| Vascular | sickle cell disease & other hemoglobinopathies, polycythemia vera & other lymphoproliferative disorders | sludging of cells in vessels |
| pregnancy | impaired venous drainage caused by the gravid uterus | |
| Infection | septic emboli | causing arterial occlusion |
| Drugs / Toxins | steroid use | fat cell enlargement causing medullary hypertension and intraosseous venous occlusion |
| alcoholism | fatty emboli causing arterial occlusion | |
| Inflammatory | pancreatitis | fatty emboli causing arterial occlusion |
| Congenital | Gaucher's disease | marrow packing by Gaucher cells causing medullary hypertension
and intraosseous venous occlusion |
| Autoimmune | systemic lupus erythematosus | vasculitis causing arterial occlusion |
| Trauma | fracture / dislocation | interruption of arterial supply to bone (e.g. scaphoid fracture, hip dislocation, talar neck fracture) |
| radiation | direct injury to vascular supply leading to occlusion | |
| dysbarism (caisson disease) |
nitrogen emboli causing arterial occlusion / accumulation of nitrogen bubbles in marrow fat | |
| thermal trauma (burns, frostbite) |
direct tissue damage | |
| Endocrine / Metabolic | Cushing's disease | cell enlargement causing medullary hypertension and intraosseous venous occlusion |
The fine, speckled soft tissue calcifications are easy to see in this patient. The differential diagnosis of soft tissue calcifications comes up frequently, and it behooves the radiologist to say something intelligent about them. Fortunately the differential diagnosis for this finding is not too difficult. Soft tissue calcifications are usually caused by one of the following six entities, listed below in order of prevalence.
|
Differential Diagnosis of |
||
| Cause | Typical Appearance | Prevalence |
| Dystrophic | small to large amorphous Ca++ in the damaged tissue -- may progress to ossification (formation of cortex and medullary space are then seen) | 95 - 98 % |
| CPPD | chondrocalcinosis; occasionally associated with calcifications in the soft tissues of the spine | 1 - 2 % |
| Metastatic calcification | finely speckled Ca++ throughout soft tissues | 1 - 2 % |
| Tumoral calcinosis | big globs of Ca++, usually near a joint | << 1 % |
| Metastatic osteosarcoma |
amorphous, fluffy, confluent collection of Ca++ |
<<< 1 % |
| Primary soft tissue osteosarcoma | amorphous, fluffy, confluent collection of Ca++ |
<<<< 1 % |
In the list above, one can see that almost every calcification seen in the soft tissues in actual radiographic practice is due to dystrophic calcification. What does this mean? Simply this: when tissue is damaged, the body responds to this injury in a nonspecific manner by invoking the generic inflammatory response reaction. This sometimes results in calcification of the damaged tissue. This calcification is often only microscopic, but is occasionally enough to be seen radiographically. Again, dystrophic calcification means damaged tissue. Any kind of damage will do. Going through the table above, we see that most of the causes listed tend to produce larger globs of calcification than those seen in this patient, other than metastatic calcification.
The diffuse, fine, speckled calcifications seen in this case are typical of those seen with "metastatic calcification". This term refers to the diffuse pattern seen throughout the soft tissues, and not necessarily to the presence of an underlying malignancy. The differential includes entities such as renal failure, hyperparathyroidism, sarcoidosis, milk-alkali syndrome, multiple lytic osseous metastases, multiple myeloma, and other causes.
Sooooo.... how does one put these two findings together? The most likely common thread is renal disease. A patient with a renal transplant would commonly be using steroids -- a major cause of osteonecrosis. Some patients with systemic lupus erythematosus (SLE) will develop renal disease. SLE can cause osteonecrosis either by itself, or due to the steroids that are sometimes used to treat it.