Biological effects and safety aspects of magnetic resonance imaging.
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Biomedical subjects
Publications and source records attributed to F G Shellock.
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High-field-strength/high-frequency magnetic resonance (MR) imaging systems can cause tissue heating. Since the eye is particularly susceptible to temperature elevations because of its relatively poor blood supply, the authors measured corneal temperatures in 33 patients immediately before and after MR imaging performed with a 1.5-T (64-MHz) imager and a transmit/receive head coil at estimated peak specific absorption rates (SAR) ranging from 2.54 to 3.05 W/kg. There was a statistically (P less than .001) significant increase in the average corneal temperature (32.7 degrees C +/- 0.7 before imaging, 33.2 degrees C +/- 0.5 after). The changes in corneal temperature ranged from 0.0 degrees C to 1.8 degrees C (mean, 0.5 degrees C), and the highest corneal temperature measured after imaging was 34.4 degrees C. In animal models, the eye temperature threshold for radio frequency-induced cataractogenesis is between 41 degrees C and 55 degrees C. The authors conclude that clinical MR imaging with use of a head coil at the SARs studied causes relatively minor increases in corneal temperature that do not appear to pose any thermal hazard to ocular tissue.
The patellofemoral joint was imaged with magnetic resonance (MR) in the axial plane while the knee was positioned from 0 degrees to 32 degrees of flexion (nine positions). These multiple sequential images obtained within the early phases of flexion of the knee were viewed in a "cine-loop" format, producing a kinematic study that clearly demonstrated the relationship of the patella to the trochlear groove. Four healthy subjects and one patient with known bilateral subluxing patellae were studied. The preliminary results suggest that kinematic MR imaging of the patellofemoral joint is potentially useful for the evaluation of patellar tracking abnormalities.
Ferromagnetic biomedical implants are considered a contraindication for MR imaging primarily because of the potential hazards associated with their movement or dislodgment. Many metallic biomedical implants are composed of nonferromagnetic materials and do not present a danger to patients during MR imaging. Therefore, to evaluate the ferromagnetic qualities of 36 different metallic biomedical implants (four aneurysm clips, six hemostatic clips, four dental implants, seven prosthetic heart valves, eight orthopedic prostheses, one artificial urinary sphincter, three contraceptive diaphragms, and three cerebral ventricular shunt tube connectors) not previously evaluated with a high-field-strength MR system, we measured deflection forces at the portal of the magnet of a 1.5-T MR system. Fourteen of the 36 metallic biomedical implants were determined to be ferromagnetic as indicated by their deflection in the static magnetic field. However, only the four aneurysm clips (Drake, Mayfield, McFadden, and Sundt-Kees) had sufficient ferromagnetism to warrant exclusion of patients with these implants from imaging with a 1.5-T MR system because of the possibility of movement or displacement. The calculated deflection forces for these aneurysm clips were comparable with previously reported values of certain aneurysm clips that have been designated to present a risk for patients undergoing MR imaging. Patients with 32 of 36 metallic biomedical implants tested can be safely imaged with high-field-strength MR systems.
Ferromagnetic metallic implants and materials are regarded as contraindications for MR imaging because of the potential risks associated with their movement or displacement. To date, 14 published articles have evaluated the ferromagnetic qualities of 127 different metallic implants and other materials, including aneurysm and hemostatic clips (32); dental implants and materials (five); intravascular coils, filters, and stents (13); ear implants (14); prosthetic heart valves (29); orthopedic implants and materials (eight); penile implants (nine); and miscellaneous metallic implants and materials (17). All of these materials were evaluated by measuring the deflection forces induced by static magnetic fields at strengths ranging from 0.147 to 4.7 T. This article is a compilation of the results of these studies; it lists all 127 of the materials tested, indicates whether they were found to be deflected by the static magnetic fields, and gives the highest static magnetic field strength at which they were evaluated. Of the metallic implants tested, 66 were nonferromagnetic, and 29 exhibited only minimal deflection relative to their in vivo applications (i.e., the deflection forces were thought to be insufficient to move or dislodge the implant or material in situ). The authors of these studies concluded that patients with these particular metallic implants or materials (95/127, 75%) can be examined safely by MR imaging with scanners having static magnetic field strengths up to and including those used for the specific evaluations. Patients with other ferromagnetic materials or implants may also undergo MR imaging safely; however, both careful consideration of the factors that influence the deflection of metallic implants and prudent clinical judgment are required before patients who have these objects are examined via MR imaging.
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Temperature, heart rate, and blood pressure responses to high-field-strength magnetic resonance (MR) imaging were studied in 50 patients who underwent procedures at exposures to radiofrequency radiation above the present recommended whole-body average specific absorption rate (SAR) of 0.4 W/kg. Body temperature significantly increased an average of 0.2 degrees C. The highest body temperature recorded after MR imaging was 37.5 degrees C. There was no significant correlation between the change (before and after imaging) in body temperature and whole-body average SARs. Changes in skin temperatures were variable, depending on anatomic site. The largest change was 3.5 degrees C, and the highest skin temperature recorded after imaging was 35.1 degrees C. There was a modest correlation between the change in skin temperatures and whole-body average SARs. Average heart rate and average mean blood pressure measured immediately before imaging were not significantly different afterward. High-field-strength MR imaging at the whole-body average SARs of 0.42-1.2 W/kg studied was not associated with any temperature- or hemodynamic-related deleterious effects.
Reports in the literature concerning the effect of static magnetic fields on the body temperature of mammals have been contradictory and confusing. A significant increase in body temperature in human subjects exposed to the static magnetic fields used in magnetic resonance imaging (MRI) would have important safety implications. Therefore, in two separate studies we determined body temperature in 20 subjects exposed to a 1.5 T static magnetic field. One group of subjects (Group I, N = 9) had sublingual pocket temperature measured immediately before and after a 60 min exposure, while another group of subjects (Group II, N = 11) had esophageal temperature determined at 2 min intervals during a 20 min exposure. No statistically significant changes in body temperature were observed in either Group I or II subjects during exposure to the 1.5 T static magnetic field. We conclude that a relatively intense static magnetic field has no effect on body temperature of normal human subjects.
Cachexia is a common manifestation of advanced cancer and frequently contributes to physical disability and mortality. An increased metabolic rate has been suggested to be one of the causes of cancer-induced cachexia, although the mechanisms producing this hypermetabolism remain unclear. The presence and activation of brown adipose tissue, a highly thermogenic tissue, may result in a hypermetabolic state and be partially responsible for weight loss in cancer patients. To investigate this hypothesis, we examined necropsy samples of peri-adrenal tissues using light microscopy to identify the prevalence of brown adipose tissue in 25 cachectic patients who died from cancer and 15 age-matched subjects who died from other illnesses. Brown adipose tissue was observed in 20 of the cancer patients (80%) compared to 2 of the age-matched subjects (13%). Therefore, our preliminary results indicate that a high prevalence of brown adipose tissue is associated with cancer-induced cachexia and may reflect an abnormal mechanism responsible for profound energy expenditure and weight loss.
Warming temperature sensitive neurons in the hypothalamus will induce thermoregulatory heat dissipation. Application of radiofrequency (RF) radiation to the head during magnetic resonance imaging (MRI) could, conceivably, heat the brain, causing a generalized peripheral vasodilation and result in a paradoxical and unnecessary decrease in body temperature. To evaluate the thermoregulatory responses to the RF power deposition used during MRI, we measured body (sublingual pocket) and skin temperatures in 15 patients immediately before and after MRI scans of the head. Ear-skin blood flow was determined by laser-Doppler velocimetry to assess local vasomotor tone. A high-field (1.5 tesla/64 MHz) MRI device (General Electric Company) with a coil designed for head/brain imaging was used in this study. Ambient conditions were room temperature 20-24 degrees C and relative humidity 40-50%. The specific absorption rate averaged over the head ranged from 0.83 to 1.20 W/kg. There was a slight but statistically significant elevation in body temperature (36.5 +/- 0.5 to 36.7 +/- 0.4 degrees C). Skin temperatures of the ear (30.0 +/- 1.2 to 32.0 +/- 0.9 degrees C) and forehead (32.4 +/- 0.5 to 32.8 +/- 0.5 degrees C) increased significantly, while hand (29.9 +/- 1.4 to 29.8 +/- 2.1) skin temperature was unchanged. Ear-skin blood flow also increased a statistically significant amount (average change 36%). The data indicate that there was predominantly surface heating associated with MRI of the head which stimulated a local vasodilating response (i.e. significant increase in ear skin blood flow).(ABSTRACT TRUNCATED AT 250 WORDS)
Current safety guidelines recommend limiting the exposure to radiofrequency (RF) radiation used for clinical magnetic resonance imaging to a whole body average specific absorption rate (SAR) of 0.4 W/kg. Since it may be desirable to image with SARs that exceed this level during MRI of the spine, we evaluated the thermal responses associated with these procedures. Body and skin temperatures were determined in 25 patients immediately before and after MRI. Since the eye is particularly susceptible to thermal injury, corneal temperature was also measured. High-resolution thermography was performed on three subjects to evaluate the surface heating pattern and identify potential thermal 'hot spots'. A 1.5 tesla/64 MHz MRI system with quadrature transmission and reception was used iN this study. The whole body average specific absorption rate ranged from 0.5 to 1.3 W/kg. Ambient conditions were room temperature 20-24 degrees C and relative humidity between 40 and 50 per cent. There was a slight but statistically significant (p less than 0.01) increase in body temperature after MRI (36.5 +/- 0.4 to 36.7 +/- 0.4 degrees C). Temperatures of the hand (30.4 +/- 1.4 to 31.2 +/- 1.0 degrees C), positioning isocenter (32.1 +/- 0.6 to 32.9 +/- 0.5), and cornea (32.5 +/- 0.6 to 32.9 +/- 0.5 degrees C) also increased a statistically significant amount. Thermographic imaging revealed normal heating patterns with no surface 'hot spots'. We conclude that the temperature changes associated with MRI of the spine at the SARs we studied were well below known thresholds for adverse effects and do not appear to be harmful to patients.
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In 14 patients with severe congestive heart failure (CHF) due to ischemic heart disease or idiopathic dilated cardiomyopathy, the hemodynamic response to intravenous infusion of dobutamine (D) was compared to that of a new non-catechol, non-glycoside, inotropic and vasodilator agent, MDL-17,043 (MDL) administered in incremental intravenous doses. D and MDL produced comparable increases in cardiac index (L/min/m2) (1.8 +/- 0.4 to 2.9 +/- 0.8 and 1.7 +/- 0.3 to 3.3 +/- 0.6, respectively; both p = 0.001) and stroke volume index (ml/beat/m2) (24 +/- 8 to 35 +/- 9 and 22 +/- 7 to 39 +/- 11, respectively; both p = 0.001). Both D and MDL reduced left ventricular filling pressure (29 +/- 5 to 24 +/- 5 and 29 +/- 6 to 17 +2- 6 mm Hg, respectively; both p less than 0.05), and mean right atrial pressure (11 +/- 4 to 8 +/- 4 and 13 +/- 5 to 6 +/- 4 mm Hg, respectively; both p = 0.001). The overall changes in heart rate and mean arterial pressure were small with both D and MDL. However, MDL in comparison to D resulted in a significantly lower left ventricular filling pressure (p = 0.001), mean pulmonary arterial pressure (p = 0.001), and mean arterial pressure (p less than 0.05). The salutary hemodynamic effects of MDL on cardiac index and left ventricular filling pressure were sustained for an average of 9.6 hours, whereas the effects of D dissipated within 30 minutes of stopping the infusion. No serious adverse effects were noted during acute administration with either drug. Therefore, intravenous MDL may be a useful substitute for D in the acute therapy of severe CHF.
Deep-body or core temperature decreases during exercise in patients with heart failure, primarily due to the circulatory inadequacies associated with the pathophysiology of this condition. Vasodilators are commonly used to treat patients suffering from heart failure because these drugs improve total cardiac output and blood-flow to the regional circulations. In heart failure patients, the core temperature response to exercise should also be affected if the circulation is improved by vasodilators. Patients with severe heart failure were studied at rest and during upright bicycle exercise before, and after, short-term treatment with vasodilators (2-minoxidil, 3-hydralazine, 5-captopril). Their heart rate increased significantly (P less than 0.05) from rest to exercise before (87 +/- 15 109 +/- 14 beats/min), and after 89 +/- 13- 112 +/- 15 beats/min) vasodilators, but there was no drug-related affect on these changes. Mean arterial and pulmonary capillary wedge pressures were significantly (P less than 0.05) decreased at rest and after the administration of vasodilators (mean arterial pressure 88 +/- 7 mmHg before; 77 +/- 8 mmHg after; pulmonary capillary wedge pressure 25 +/- 8 mmHg before, 19 +/- 9 mmHg after). During exercise, the increases in mean arterial and pulmonary capillary wedge pressures were not significantly different from the before vasodilator values (mean arterial pressure 92 +/- 14 mmHg before, 87 +/- 14 mmHg after; pulmonary capillary wedge pressure 31 +/- 11 mmHg before, 29 +/- 11 mmHg after). Vasodilators increased cardiac output significantly (P less than 0.05) at rest (3.1 +/- 0.6 litre/min to 4.1 +/- 1.1 litre/m) and during exercise (4.8 +/- .2 litre/min-5.6 +/- 1.7 litre/min). The core temperature (mixed venous blood temperature) decreased significantly (P less than 0.05) during exercise from 37.04 +/- 0.62 degrees C to 36.65 +/- 0.65 degrees C, before treatment with vasodilators. After administration of vasodilators, resting core temperature was not significantly different (36.95 +/- 0.54 degrees C) and still decreased significantly (P less than 0.05) during exercise to 36.73 +/- 0.53 degrees C. This decrease was significantly (P less than 0.05) different from the core temperature response before the administration of vasodilators. We conclude that heart failure patients, treated with short-term vasodilators, have an attenuation of the core temperature response that typically occurs during exercise. This change in the core temperature response is the result of the vasodilator-induced improvement in circulation.
Core temperature decreases throughout short-term maximal exercise in heart-failure patients. To investigate possible causes for this unusual response to exercise, we studied core (pulmonary arterial blood), femoral vein, muscle, and skin temperatures in eight patients with severe heart failure who performed maximal upright incremental bicycle exercise to 50 W. A normal group (n = 4) was exercised for comparison. In the heart-failure patients, core temperature was 36.95 +/- 0.37 degrees C at rest, significantly (P less than 0.05) decreased at 25 W of exercise to 36.59 +/- 0.40 degrees C, and at 50 W remained decreased to 36.57 +/- 0.40 degrees C. In comparison, we found that the resting core temperature in the normal subjects was 37.28 +/- 0.34 degrees C, was the same at 25 W (37.29 +/- 0.41 degrees C), and increased significantly (P less than 0.05) to 37.50 +/- 0.32 degrees C at 50 W of exercise. Femoral vein temperature in heart-failure patients (n = 6) was below core temperature throughout exercise to 25 and 50 W (36.22 +/- 0.62 and 36.34 +/- 0.65 degrees C, respectively). Muscle temperature (n = 7) was significantly (P less than 0.05) lower in the heart-failure patients (34.8 +/- 1.1 degrees C) at rest compared with the normal subjects (36.2 +/- 1.0 degrees C). During exercise, muscle temperature increased above core temperature in only four of the heart-failure patients and was significantly (P less than 0.05) lower (36.5 +/- 1.3 degrees C) compared with the normal subjects (38.0 +/- 0.2 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)
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