Diagnosing brain death by CT perfusion and multislice CT angiography.

INTRODUCTION: Although the diagnosis of brain death (BD) is usually based on clinical criteria, in sedated patients, ancillary techniques are needed. This study was designed to assess the accuracy of cerebral multislice computed tomographic angiography (CTA) and CT perfusion (CTP) in diagnosing BD. METHODS: Prospective observational study in 27 BD patients. RESULTS: All patients were diagnosed as BD based on clinical and electroencephalogram findings. After BD diagnosis, CTP was performed followed by 64-detector multislice CTA from the aortic arch to the vertex. Images were reconstructed from 0.5 mm sections. In 24 patients, a lack of cerebral blood flow (CBF) was detected by CTP, and CTA revealed luminal narrowing of the internal carotid artery in the neck and absence of anterior and posterior intracranial circulation (sensitivity 89%). CTA detected CBF exclusively in extracranial portions of the internal carotid and vertebral arteries. Two patients with anoxic brain injury and decompressive craniectomy showed CBF in the CTA such that the CTP results were considered false negatives, given BD had been confirmed by clinical and EEG findings, along with evoked potentials. In one clinically BD patient, in whom an alpha rhythm was detected in the electroencephalogram, CBF was only observed in the intracranial internal carotid with no posterior circulation noted. This patient was therefore considered exclusively brain stem dead. CONCLUSIONS: The radiological protocol used shows a high sensitivity and excellent specificity for detecting the cerebral circulatory arrest that accompanies BD. As a rapid, non-invasive, and widely available technique it is a promising alternative to conventional 4-vessel angiography.

Mechanical ventilation causes monocyte deactivation in intact and endotoxin-treated mice.

BACKGROUND: Monocyte deactivation, defined as the decrease of surface expression of class II molecules of the main histocompatibility complex (MHC) on circulating monocytes, can occur after severe injuries, like trauma, sepsis, or major surgery. We hypothesized that mechanical ventilation could also be a cause. METHODS: Prospective experimental study. Intact and endotoxin-treated (20 mg/kg of intraperitoneal lipopolysaccharide, 4 hours before the experiment) Swiss mice were tracheotomized and ventilated with one of four possible ventilatory settings: control (no ventilation), low pressure (peak pressure 20 cm H2O, positive end-expiratory pressure [PEEP] 4 cm H2O), high pressure (peak pressure 30 cm H2O, PEEP 0 cm H2O), or high pressure plus an intraperitoneal dose of interferon (IFN)-gamma (40,000 units). After 1 hour, an arterial blood sample was obtained, and the right lung removed to measure gas exchange and the lung wet-to-dry weight ratio. Expression of class II MHC molecules was assessed in peripheral monocytes using flow cytometry. RESULTS: High-pressure ventilation was related to a decrease in oxygenation and to an increase in lung wet-to-dry weight ratio. The expression of class II MHC molecules in blood monocytes decreased in the high-pressure group, but not in IFN-gamma-treated mice. The results were similar in both intact and endotoxin-treated mice. CONCLUSIONS: Mechanical ventilation with high pressure and zero PEEP can cause monocyte deactivation. This phenomenon can be avoided by treatment with IFN-gamma.