Imaging of the apparent diffusion coefficient for the evaluation of cerebral metabolic recovery after cardiac arrest

• Published in: Magnetic resonance imaging 1995, Vol.13 (6), p.781-790
• Main Authors: Fischer, Matthias, Bockhorst, Kurt, Hoehn-Berlage, Mathias, Schmitz, Bernd, Hossmann, Konstantin-Alexander
• Format: Article
• Language: English
• Subjects: ADC; Animals; Biological and medical sciences; Brain - metabolism; Brain Ischemia - metabolism; Brain Ischemia - physiopathology; Cardiac arrest; Cats; Cerebral metabolism; Diffusion-weighted NMR imaging; Electrocardiography; Electroencephalography; Heart Arrest - metabolism; Heart Arrest - physiopathology; Investigative techniques, diagnostic techniques (general aspects); Magnetic Resonance Spectroscopy; Male; Medical sciences; Nervous system; Pneumatic vest; Radiodiagnosis. Nmr imagery. Nmr spectrometry; Resuscitation
• ISSN: 0730-725X; 1873-5894
• DOI: 10.1016/0730-725X(95)00030-K

The apparent diffusion coefficient (ADC) of water is a sensitive indicator of water and ion homeostasis of brain. Resuscitation of the brain after cardiac arrest, the most frequent reason for global cerebral ischemia under clinical conditions, depends critically on the reversal of disturbances of water and ion homeostasis. We, therefore, investigated whether ADC imaging can be used to monitor the development and reversal of ischemic brain injury during and after cardiac arrest. Ten adult mongrel normothermic cats were anesthetized with alfentanil and midazolam, immobilized with pancuronium, and mechanically ventilated with O 2 N 2O . Arterial, left ventricular, central venous, and intracranial pressures were monitored throughout the experiment. Magnetic resonance imaging was performed in a 4.7T MR scanner with a shielded gradient system. Diffusion-weighted images (DWI) were obtained by pulsed gradient spin echoes (diffusion weighting factor b: 0, 500, 1000, 1500 s/mm 2). Quantitative ADC images were calculated from DWIs by fitting signal intensities against b-factors. Fifteen minute cardiac arrest was induced in the magnet by electrical fibrillation. Resuscitation was also carried out in the magnet, using a pneumatic vest for remotely controlled closed chest cardiac massage. Seven of 10 animals were resuscitated successfully and subsequently monitored for 3 h. During cardiac arrest, ADC declined from 678 ± 79 × 10 −6 to 430 ± 128 × 10 −6 mm 2/s (63% of baseline). In the successfully resuscitated animals ADC returned to 648 ± 108 × 10 −6 mm 2/s within 30 min and remained at this level throughout the 3 h of recirculation. Regional evaluations of ADC revealed a transient overshoot in brainstem and basal ganglia to 114% of control at 15 min before returning to baseline values after 40 min. Failure of cardiac resuscitation prevented ADC normalization and led to its further decline to below 50% of control. Postcardiac arrest normalization of ADC maps correlated with homogeneous return of ATP, glucose, and lactate to near normal, whereas failure of ADC normalization was associated with depletion of ATP and glucose and severe lactate accumulation. In conclusion, our data indicate, that normalization of ADC is a reliable indicator of cerebral recovery after resuscitation from cardiac arrest.