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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. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study is to assess the incidence of sublingual microcirculatory flow alterations, according to a predefined arbitrary cutoff value, in patients with 'clinical signs of impaired organ perfusion'. Secondary endpoints were the changes in microvascular flow index (MFI), 'clinical signs of impaired organ perfusion', and stroke volume (SV) after fluid administration, and the differences between groups. Methods: Prospective, single-center, observational study in a 22-bed mixed intensive care unit (ICU). Patients ≥18 years with invasive hemodynamic monitoring and 'clinical signs of impaired organ perfusion' as the principal reason for fluid administration were included. Before and after fluid challenge, systemic hemodynamics and direct in vivo observation of the sublingual microcirculation with sidestream dark-field imaging were obtained. Microvascular flow index (MFI) <2.6 was predefined as abnormal. Results: N = 50. At baseline, MFI <2.6 was present in 66 % of the patients. In these patients, MFI increased from 2.3 (2-2.5) at baseline to 2.5 (2.1-2.8) after fluid challenge ( p = 0.003). This was accompanied by a reduction in the number of 'clinical signs of impaired organ perfusion' from 2 (1-2) to 1 (0-2) ( p < 0.001). However, in patients with MFI >2.6 at baseline, MFI and clinical signs changed insignificantly [2.8 (2.8-2.9) versus 2.8 (2.7-3), p = 0.45, respectively, 1 (1-2) versus 1 (1-2), p < 0.32]. These changes were not restricted to patients with a rise in SV ≥10 %. Conclusions: These data add to the understanding that noninvasive assessment of microvascular blood flow may help to identify patients eligible for fluid therapy, and to evaluate its effect. [ABSTRACT FROM AUTHOR]

Purpose: A fall in tissue oxygen tension (tPO) is an early indicator of organ hypoxia in both patients and animal models. We previously demonstrated the utility of bladder tPO in various rodent shock models. As a prelude to clinical testing, we aimed to provide further validation of bladder tPO monitoring in a large animal model undergoing a range of cardiorespiratory insults and vasoactive drug interventions. Methods: Anaesthetized, mechanically ventilated, instrumented female pigs ( n = 8) were subjected to a range of short-term cardiorespiratory (changes in inspired oxygen concentration (FiO), haemorrhage, positive end-expiratory pressure) and pharmacologic (inotrope, pressor) challenges. Global haemodynamics, arterial and pulmonary blood gases and bladder tPO were measured before and after each challenge. Results: Bladder tPO values fell in line with increasing degrees of hypoxaemia and haemorrhage, and were restored during resuscitation. These changes often preceded those seen in global haemodynamics, arterial base excess and lactate. The rise in bladder tPO with hyperoxia, performed as an oxygen challenge test, was incrementally blunted by progressive haemorrhage. Dobutamine and norepinephrine both increased cardiac output and global O delivery, but had no effect on bladder tPO or lactataemia in these healthy pigs. Conclusions: In this pig model bladder tPO provides a sensitive indicator of organ hypoxia compared to traditional biochemical markers during various cardiorespiratory challenges. This technique offers a potentially useful tool for clinical monitoring. [ABSTRACT FROM AUTHOR]

Purpose: The clinical use of vasoactive drugs is not only intended to improve systemic hemodynamic variables, but ultimately to attenuate derangements in organ perfusion and oxygenation during shock. This review aims (1) to discuss basic physiology with respect to manipulating vascular tone and its effect on the microcirculation, and (2) to provide an overview of available clinical data on the relation between vasoactive drugs and organ perfusion, with specific attention paid to recent developments that have enabled direct in vivo observation of the microcirculation and concepts that have originated from it. Methods: A MedLine search was conducted for clinical articles in the English language over the last 15 years pertainig to shock, sepsis, organ failure, or critically ill patients in combination with vasoactive drugs and specific variables of organ perfusion/oxygenation (e.g., tonometry, indocyanine clearance, laser Doppler, and sidestream dark field imaging). Results: Eighty original papers evaluating the specific relationship between organ perfusion/oxygenation and the use of vasoactive drugs were identified and are discussed in light of physiological theory of vasomotor tone. Conclusions: Solid clinical data in support of the idea that increasing blood pressure in shock improves microcirculatory perfusion/oxygenation seem to be lacking, and such a concept might not be in line with physiological theory of microcirculation as a low-pressure vascular compartment. In septic shock no beneficial effect on microcirculatory perfusion above a mean arterial pressure of 65 mmHg has been reported, but a wide range in inter-individual effect seems to exist. Whether improvement of microcirculatory perfusion is associated with better patient outcome remains to be elucidated. [ABSTRACT FROM AUTHOR]