A decision to withdraw life-sustaining treatment (WLST) is derived by a conclusion that further treatment will not enable a patient to survive or will not produce a functional outcome with acceptable quality of life that the patient and the treating team regard as beneficial. Although many hospitalized patients die under such circumstances, controlled donation after the circulatory determination of death (cDCDD) programs have been developed only in a reduced number of countries. This International Collaborative Statement aims at expanding cDCDD in the world to help countries progress towards self-sufficiency in transplantation and offer more patients the opportunity of organ donation. The Statement addresses three fundamental aspects of the cDCDD pathway. First, it describes the process of determining a prognosis that justifies the WLST, a decision that should be prior to and independent of any consideration of organ donation and in which transplant professionals must not participate. Second, the Statement establishes the permanent cessation of circulation to the brain as the standard to determine death by circulatory criteria. Death may be declared after an elapsed observation period of 5 min without circulation to the brain, which confirms that the absence of circulation to the brain is permanent. Finally, the Statement highlights the value of perfusion repair for increasing the success of cDCDD organ transplantation. cDCDD protocols may utilize either in situ or ex situ perfusion consistent with the practice of each country. Methods to accomplish the in situ normothermic reperfusion of organs must preclude the restoration of brain perfusion to not invalidate the determination of death.

We have compared the effect of increasing optode separation (range 0.7-5.5 cm) on the sensitivity of near infrared spectroscopy (NIRS) to discrete reductions in scalp and cerebral oxygenation in 10 healthy men (mean age 32, range 26-39 yr) using multichannel NIRS. During cerebral oligaemia (a mean reduction in middle cerebral artery flow velocity of 47%) induced by a mean reduction in end-tidal PCO2 of 2.4 kPa, the decrease in oxyhaemoglobin detected by NIRS became significantly greater with increasing optode separation (P < 0.0001). In response to scalp hyperaemia induced by inflation and release of a pneumatic scalp tourniquet, increases in oxyhaemoglobin became significantly smaller with increasing optode separation (P < 0.0002). These results are consistent with theoretical models of the behaviour of NIR light in the adult head and support the concept of using multi-detector NIRS to separate intra- and extracranial NIR signal changes. However, the emitter-detector separation used by currently available cerebral oximeters is not large enough to provide optimal spatial resolution.

We have studied the effects of extracranial ischaemia and intracranial hypoxia on measurement of cerebral oxygenation using near-infrared, reflectance-mode, cerebral oximetry (Invos 3100 cerebral oximeter) in healthy adult subjects. Under stable systemic conditions, scalp ischaemia induced by a pneumatic tourniquet caused an apparent reduction in mean regional cerebral oxygenation (rSO2) from mean 72 (SD 6)% to 59 (7)% (n = 8, P < 0.001). rSO2 returned to control values within 1 min of release of the tourniquet. Local scalp ischaemia induced by rapid frontalis muscle exercise caused a significant reduction (4.5 (2)% in rSO2 (n = 12, P < 0.001). The effect of systemic hypoxia on rSO2 was examined during controlled scalp ischaemia. A decrease in mean SpO2 from 98 (2)% to 66 (6)% was associated with a decrease in mean rSO2 from 57 (4)% to 41 (6)%. There was a significant correlation between the percentage reduction in rSO2 and SpO2 during hypoxia (r = 0.81, P < 0.001). We conclude that the Invos cerebral oximeter was capable of detecting tissue hypoxia deep to the scalp under carefully controlled conditions but that it also was affected significantly by changes in extracranial blood flow and oxygenation which may affect its reliability in clinical practice. Further work is necessary to define those situations in which cerebral oximetric monitoring is useful and valid.

The detection of increased cerebral oxygenation secondary to cerebral hyperaemia, induced by hypercapnia has been studied in anaesthetised patients using a near infrared, reflectance mode, cerebral oxygenation monitor (Invos 3100 Somanetics, Troy, Michigan, USA). Two studies were performed, with and without a pneumatic scalp tourniquet, to distinguish between extracranial and intracranial changes in tissue oxygenation. In the control study a mean increase in end tidal CO2 of 23-1 mm Hg was accompanied by a mean increase in middle cerebral artery flow velocity of 116%. Regional cerebral oxygen saturation (rSo,) measured transcutaneously in the frontal distribution of the middle cerebral artery increased significandy from 70*5% to 74*6% (p = 0.001). During the second study with a scalp tourniquet inflated to maintain the extracranial tissues in a state of stable ischaemia a mean increase in end tidal CO2 of 22-3 mm Hg was accompanied by a mean increase in middle cerebral artery flow velocity of 121%. The change in rSo2 from 62-6% to 64-5% was not significant (p = 0.085).There was no correlation between the change in middle cerebral artery flow velocity and rSo2 in the control or scalp ischaemia group. This study shows that the Invos 3100 monitor is sensitive to tissue oxygenation but does not reliably detect changes in cerebral oxygenation as a result of profound cerebral hyperaemia. The contribution of extracerebral tissue to the attenuation of near infrared light and the lack of spatial resolution remain major problems to be overcome before this or other near infrared spectroscopy instruments can be introduced into clinical practice.(