Lutzker L G, Alavi A
Semin Nucl Med. 1976 Jan;6(1):83-93. doi: 10.1016/s0001-2998(76)80038-4.
Sickling of erythrocytes in patients with S-hemoglobin causes marrow and bone infarction. The former can be demonstrated as a lack of 99mTc-sulfur colloid uptake on marrow imaging examination. These defects may resolve or persist long after the acute episode. If the bone is involved in the acute episode, imaging within the first few days of onset of symptoms can show lack of 99mTc-labeled phosphate uptake, usually in a smaller area than that shown by marrow scanning. Follow-up bone imaging shows increased activity, particularly along the circumference of the bone where periosteal reaction can be demonstrated radiographically. Magnification by use of the pinhole collimator provides better definition of the uptake defect and the distribution of the increased reactive uptake. Timing of examination is important. If marrow imaging is performed in an asymptomatic period, the repeat examination during a painful crisis permits differentiation of old and acute marrow infarction. If 99mTc-phosphate imaging is performed after about 2 days of symptoms, acute infarction can be differentiated from osteomyelitis, which it may mimic clinically. Although osteomyelitis may cause no increased activity in the first 48 hr after onset of symptoms, it is characterized by intense focal activity thereafter (see article by Handmaker in this issue). To assist in differentiating bone infection in a site of marrow infarction demonstrated by marrow imaging, serial bone imaging with magnification may be useful. The uptake defect, followed in several days to 2 weeks, by circumferential increased activity, is a different pattern than the homogeneously intense activity of osteomyelitis, but the peripheral distribution may not be apparent on routine imaging. It is hoped that the utilization of these techniques can decrease the emotional and economic costs of prolonged hospitalization for suspected infection and can also expand our knowledge of the complex pathophysiologic changes of sickle cell bone disease.
携带S型血红蛋白的患者红细胞镰变会导致骨髓和骨梗死。前者在骨髓显像检查中可表现为99mTc-硫胶体摄取缺乏。这些缺损在急性发作后可能会消退或长期存在。如果在急性发作时累及骨骼，症状发作后的头几天内进行的显像可显示99mTc标记的磷酸盐摄取缺乏，通常受累面积小于骨髓扫描所示。后续的骨显像显示活性增加，尤其是在骨周缘，在X线片上可显示骨膜反应。使用针孔准直器放大可更好地显示摄取缺损及反应性摄取增加的分布情况。检查时机很重要。如果在无症状期进行骨髓显像，在疼痛危象期间重复检查可区分陈旧性和急性骨髓梗死。如果在症状出现约2天后进行99mTc-磷酸盐显像，可将急性梗死与骨髓炎区分开来，骨髓炎在临床上可能与之相似。虽然骨髓炎在症状发作后的头48小时内可能不会导致活性增加，但此后其特征是局灶性活性增强（见本期Handmaker的文章）。为了协助鉴别骨髓显像显示的骨髓梗死部位的骨感染，连续放大骨显像可能有用。摄取缺损在数天至2周后出现骨周缘活性增加，这与骨髓炎均匀的强烈活性不同，但在常规显像上可能看不到外周分布。希望这些技术的应用能够降低因疑似感染而长期住院的情感和经济成本，同时也能拓展我们对镰状细胞骨病复杂病理生理变化的认识。
