Multiple myeloma: evaluation by CT

Although patients who have multiple myeloma usually have straightforward clinical symptoms and corroborative radiographs, in some instances, these patients will present atypically, with symptoms suggesting active disease but radiographs that are normal or nonspecific. We reviewed the records of 32 patients who had documented multiple myeloma and had undergone CT examinations, assessing the value of those examinations. Although CT is not indicated in all patients who have multiple myeloma, it is especially useful in patients who have bone pain and normal or nonspecific radiographs. CT provided confirmatory information in all cases in which lesions were seen on radiographs. CT also frequently demonstrated a greater extent of disease than could be appreciated on the radiographs.     

Supraacetabular insufficiency fractures

Insufficiency fractures in the supraacetabular region were identified in five women, aged 55-83 years. Factors contributing to the diminished resistance of their bones included postmenopausal osteoporosis, steroid therapy, radiation therapy, and rheumatoid arthritis. The supraacetabular fractures were seen on routine radiographs as hazy bands of sclerosis located immediately above and parallel to the acetabular roof. All five patients had additional fractures in the spine or pelvis. Supraacetabular insufficiency fractures may be an unsuspected cause of hip pain, especially in older women.     

Ferromagnetic materials in patients: detection before MR imaging

A number of surgical clips and other metallic materials embedded within patients have ferromagnetic properties that present a potential hazard when in the strong fields associated with magnetic resonance imaging. Several types of magnetometers and metal detectors were investigated as possible pre-imaging screening devices. The sensitivities and costs of these devices are given.     

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Current aspects of forensic lawFrom October 2004 to March 2005

     

Renal sympathetic and cardiac changes associated with anaphylactic hypotension

Severe anaphylactic reactions can result in life-threatening hypotension, but little is known about the autonomic changes that accompany the hypotensive response. The aim of this study was to determine the renal sympathetic and cardiac responses to anaphylactic hypotension, and to evaluate the contribution of sinoaortic and vagal afferent inputs in producing these responses. Rats were sensitized with bovine serum albumin (BSA) and, after 10-14 days, were anaesthesized with sodium pentobarbitone and arterial pressure, heart rate (HR), and renal sympathetic nerve activity (RSNA) were recorded. In about two thirds of the rats, injection of BSA evoked a severe and sustained hypotension, while in the remainder, there was either a more transient hypotension or else no significant change in arterial pressure. In control unsensitized rats, BSA injection had no significant effect on arterial pressure, heart rate, or RSNA. The BSA-induced hypotension in sensitized rats was associated with increases in HR and RSNA, the magnitudes of which were correlated with the magnitude of the hypotension. There were two components to the cardiac and renal sympathoexcitatory response: (1) an initial increase in HR and RSNA, which immediately followed the onset of hypotension and which was abolished by sinoaortic denervation and vagotomy, and (2) a delayed and gradual increase in HR and RSNA, which continued even while the arterial pressure was recovering and was reduced but not abolished by sinoaortic denervation and vagotomy. Thus, BSA-induced anaphylactic hypotension causes prolonged tachycardia and renal sympathoexcitation, which is only partly due to reflex effects arising from sinoaortic baroreceptors and cardiopulmonary receptors.     

Evidence that venoconstriction reverses the phase II sympathoinhibitory and bradycardic response to haemorrhage

Severe hypotensive haemorrhage results in a biphasic response, characterized by an initial increase in heart rate and sympathetic vasomotor activity (phase I) followed by a life-threatening hypotension, accompanied by profound sympathoinhibition and bradycardia (phase II). The phase II response is believed to be dependent on inputs from cardiopulmonary receptors, and may be triggered by the reduction in venous return and cardiac filling associated with severe haemorrhage. In this study, we tested the hypothesis that the phase II response could be reversed by venoconstriction, which is known to enhance venous return and cardiac filling, by comparing the effects of phenylephrine (which constricts veins as well as arterioles) with that of vasopressin (which constricts arterioles but not veins). In sodium pentobarbitone-anaesthetised rats, haemorrhage evoked an initial increase in heart rate (HR) and renal sympathetic activity (RSNA) followed by a large decrease in both variables to levels below the pre-haemorrhage baseline levels (phase II response). During the phase II response, an intravenous injection of phenylephrine, sufficient to restore mean arterial pressure to the pre-haemorrhage level, resulted in a gradually developing increase (over 3-4 min) in HR and RSNA back to the baseline levels. In contrast, intravenous injection of an equipressor dose of vasopressin did not result in any increase in RSNA and only a transient increase in HR. Injection of phenylephrine, but not vasopressin, also increased the pulsatile component of central venous pressure, indicative of reduced venous capacitance. The findings indicate that venoconstriction reverses the phase II sympathoinhibition and bradycardia.