The most popular of the staging systems for AVN is that of Ficat and Arlet,35 modified to include preclinical and preradiologic stages of the disease.34 This modification is important because the disease can be present in the absence of clinical and radiologic signs (stage 0). In stage I and stage II disease, the joint remains normal and the femoral head is spherical (Fig. 3.79):
Stage 0: Diagnosed on the basis of scintigraphic or MR imaging when a painful contralateral hip is being evaluated. There are no clinical or radiographic changes found. There is a double-line sign on the MR image in the asymptomatic hip in this stage.
Stage I: The trabeculae appear normal or slightly porotic. MR imaging may show a single line on T1-weighted images and the double line sign on FS PD FSE images. The double-line sign is specific and pathognomonic for AVN. The hyperintensity at the periphery of the necrotic focus is probably caused by hypervascular granulation tissue, a hyperemic response adjacent to thickened trabeculae.27 Pathologic specimens from lesions in these early stages show viable bone on necrotic bone with marrow spaces infiltrated by mononuclear cells and histiocytes, explaining the imaging changes.
Stage II: There is sclerosis and porosis of the trabeculae, and a shell of reactive bone demarcates the area of infarct. Within this area, the trabeculae and marrow spaces are acellular. There may be an extended pattern of associated marrow edema from the nonischemic region of the femoral head into the femoral neck (Fig. 3.80).
Stage III: The onset of stage III disease is marked by the loss of the spherical shape of the femoral head (Fig. 3.81). The AP radiograph may appear normal, but the lateral view often reveals a crescent sign, or radiolucency, under the subchondral bone. This represents a fracture between the subchondral bone and the underlying femoral head (Fig. 3.82). The crescent sign is the earliest indication of mechanical failure from accumulated stress fractures of nonrepaired necrotic trabeculae.27 At this stage, there is also separation of the subchondral plate from the underlying necrotic cancellous bone. The necrotic area becomes radiodense (Fig. 3.83) as a result of mineral deposition in the marrow spaces. The joint space remains preserved or may actually increase in height.
Stage IV: The femoral head undergoes further collapse, leading to articular cartilage destruction and joint space narrowing (Fig. 3.84). Segmental collapse and subchondral fracture may result in pain and disability. Frequently this is the stage at which the patient presents for evaluation, although attention is sometimes sought earlier. Pain may be attributed to increased intraosseous pressure and microfractures.
Спасибо! Я скажу, что смущает. Отсутствие опыта. Глаз ещё не наметанный! Есть постоянные сомнения в том, что патология правильно определена. В МРТ новичок. До этого случая AVN видел только один раз. Да и тот пациент был молодой и картинка была более красочная - классическая. Здесь же очень всё как-то "некротизировано". Кстати, насчет стадии. Здесь колеблюсь между III и IV стадиями с обеих сторон. Как Вы считаете?
Так и не получается у меня увеличить картинки. Виноват! Извиняюсь.
Почему-то у меня малюсенькая картиночка. Не могу ее увеличить.
Non progrĕdi est regrĕdi.
Добавил увеличенные изображения.
А в чем трудности? Что Вас смущает? все достаточно однозначно
Ficat and Arlet Staging System
The most popular of the staging systems for AVN is that of Ficat and Arlet,35 modified to include preclinical and preradiologic stages of the disease.34 This modification is important because the disease can be present in the absence of clinical and radiologic signs (stage 0). In stage I and stage II disease, the joint remains normal and the femoral head is spherical (Fig. 3.79):
Stage 0: Diagnosed on the basis of scintigraphic or MR imaging when a painful contralateral hip is being evaluated. There are no clinical or radiographic changes found. There is a double-line sign on the MR image in the asymptomatic hip in this stage.
Stage I: The trabeculae appear normal or slightly porotic. MR imaging may show a single line on T1-weighted images and the double line sign on FS PD FSE images. The double-line sign is specific and pathognomonic for AVN. The hyperintensity at the periphery of the necrotic focus is probably caused by hypervascular granulation tissue, a hyperemic response adjacent to thickened trabeculae.27 Pathologic specimens from lesions in these early stages show viable bone on necrotic bone with marrow spaces infiltrated by mononuclear cells and histiocytes, explaining the imaging changes.
Stage II: There is sclerosis and porosis of the trabeculae, and a shell of reactive bone demarcates the area of infarct. Within this area, the trabeculae and marrow spaces are acellular. There may be an extended pattern of associated marrow edema from the nonischemic region of the femoral head into the femoral neck (Fig. 3.80).
Stage III: The onset of stage III disease is marked by the loss of the spherical shape of the femoral head (Fig. 3.81). The AP radiograph may appear normal, but the lateral view often reveals a crescent sign, or radiolucency, under the subchondral bone. This represents a fracture between the subchondral bone and the underlying femoral head (Fig. 3.82). The crescent sign is the earliest indication of mechanical failure from accumulated stress fractures of nonrepaired necrotic trabeculae.27 At this stage, there is also separation of the subchondral plate from the underlying necrotic cancellous bone. The necrotic area becomes radiodense (Fig. 3.83) as a result of mineral deposition in the marrow spaces. The joint space remains preserved or may actually increase in height.
Stage IV: The femoral head undergoes further collapse, leading to articular cartilage destruction and joint space narrowing (Fig. 3.84). Segmental collapse and subchondral fracture may result in pain and disability. Frequently this is the stage at which the patient presents for evaluation, although attention is sometimes sought earlier. Pain may be attributed to increased intraosseous pressure and microfractures.
Спасибо! Я скажу, что смущает. Отсутствие опыта. Глаз ещё не наметанный! Есть постоянные сомнения в том, что патология правильно определена. В МРТ новичок. До этого случая AVN видел только один раз. Да и тот пациент был молодой и картинка была более красочная - классическая. Здесь же очень всё как-то "некротизировано". Кстати, насчет стадии. Здесь колеблюсь между III и IV стадиями с обеих сторон. Как Вы считаете?
По мне это переход из 3 в 4ю...
Опыт - это придет)
Спасибо! Здрово помогли!