OBJECTIVE Elder abuse is underrecognized, and identification of subtle cases requires a high index of suspicion among all health care providers. Because many geriatric injury victims undergo radiographic imaging, diagnostic radiologists may be well positioned to identify injury patterns suggestive of abuse. Little is known about radiologists’ experience with elder abuse. Our goal was to describe knowledge, attitudes, training, and practice experience in elder abuse detection among diagnostic radiologists. SUBJECTS AND METHODS We conducted 19 interviews with diagnostic radiologists at a large urban academic medical center using a semistructured format. Data from these sessions were coded and analyzed to identify themes. RESULTS Only two radiologists reported any formal or informal training in elder abuse detection. All subjects believed they had missed cases of elder abuse. Even experienced radiologists reported never having received a request from a referring physician to assess images for evidence suggestive of elder abuse. All subjects reported a desire for additional elder abuse training. Also, subjects identified radiographic findings or patterns potentially suggestive of elder abuse, including high-energy injuries such as upper rib fractures, injuries in multiple stages of healing, and injuries inconsistent with reported mechanism. CONCLUSION Radiologists are uniquely positioned to identify elder abuse. Though training in detection is currently lacking, providers expressed a desire for increased knowledge. In addition, radiologists were able to identify radiographic findings suggestive of elder abuse. On the basis of these findings, we plan to conduct additional studies to define pathognomonic injury patterns and to explore how to empower radiologists to incorporate detection into their practice.

The effect of adenosine on the respiratory burst was investigated using human neutrophils adherent to serum-coated surfaces. Adenosine caused complete suppression of the respiratory burst elicited by TNF-alpha, FMLP, or CSF for granulocytes; partial suppression of the response to CSF for granulocytes/macrophages, Staphylococcus aureus, Escherichia coli, Listeria monocytogenes, or uncoated polystyrene surfaces; and no suppression of the response to PMA. In most experiments, 4.7 x 10(-7) M and 2.5 x 10(-8) M adenosine caused 50% suppression of H2O2 release in response to TNF-alpha and FMLP, respectively, and 10 microM caused 100% suppression. Preexposure of neutrophils to ADP blocked the inhibitory effect of adenosine. With adherent neutrophils, there is a prolonged lag period in the onset of the respiratory burst in response to cytokines. Adenosine was fully suppressive if its addition was delayed past the first third of this lag period, or if it was removed during the last third of the lag period. A 10-min pulse with adenosine was most inhibitory when delivered in the middle third of the lag period. Dihydrocytochalasin B abolished the suppressive effect of adenosine on H2O2 release in response to FMLP. Thus adenosine, at concentrations found in human plasma, is a potent but selective inhibitor of the respiratory burst of adherent human neutrophils in response to physiologic, soluble stimuli, and ADP is a potentially physiologic counter-suppressant. Adenosine appears to exert most of its effect during a discrete interval within the lag period before onset of the respiratory burst, and may affect the coupling of agonist receptors to the cytoskeleton.