Annals of intensive care
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Annals of intensive care · Jan 2011
Microcirculatory alterations: potential mechanisms and implications for therapy.
Multiple experimental and human trials have shown that microcirculatory alterations are frequent in sepsis. In this review, we discuss the characteristics of these alterations, the various mechanisms potentially involved, and the implications for therapy. Sepsis-induced microvascular alterations are characterized by a decrease in capillary density with an increased number of stopped-flow and intermittent-flow capillaries, in close vicinity to well-perfused capillaries. ⋯ Other agents can markedly improve the microcirculation, including activated protein C and antithrombin, vitamin C, or steroids. In conclusion, microcirculatory alterations may play an important role in the development of sepsis-related organ dysfunction. At this stage, therapies to target microcirculation specifically are still being investigated.
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Annals of intensive care · Jan 2011
Corticosteroids for severe sepsis: an evidence-based guide for physicians.
Septic shock is characterized by uncontrolled systemic inflammation that contributes to the progression of organ failures and eventually death. There is now ample evidence that the inability of the host to mount an appropriate hypothalamic-pituitary and adrenal axis response plays a major in overwhelming systemic inflammation during infections. Proinflammatory mediators released in the inflamed sites oppose to the anti-inflammatory response, an effect that may be reversed by exogenous corticosteroids. ⋯ Corticosteroids should be initiated only in patients with sepsis who require 0.5 μg/kg per minute or more of norepinephrine and should be continued for 5 to 7 days except in patients with poor hemodynamic response after 2 days of corticosteroids and with a cortisol increment of more than 250 nmol/L after a standard adrenocorticotropin hormone (ACTH) test. Hydrocortisone should be given at a daily dose of 200 mg and preferably combined to enteral fludrocortisone at a dose of 50 μg. Blood glucose levels should be kept below 150 mg/dL.
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Annals of intensive care · Jan 2011
Postcardiac arrest syndrome: from immediate resuscitation to long-term outcome.
The prognosis for postcardiac arrest patients remains very bleak, not only because of anoxic-ischemic neurological damage, but also because of the "postcardiac arrest syndrome," a phenomenon often severe enough to cause death before any neurological evaluation. This syndrome includes all clinical and biological manifestations related to the phenomenon of global ischemia-reperfusion triggered by cardiac arrest and return of spontaneous circulation. The main component of the postcardiac arrest syndrome is an early but severe cardiocirculatory dysfunction that may lead to multiple organ failure and death. ⋯ Therapeutic hypothermia is now the cornerstone of postanoxic cerebral protection. Its widespread use is clearly recommended, with a favorable risk-benefit ratio in selected population. Neuroprotection also is based on the prevention of secondary cerebral damages, pending the results of ongoing therapeutic evaluations regarding the potential efficiency of new therapeutic drugs.
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Annals of intensive care · Jan 2011
Variability in the pediatric intensivists' threshold for withdrawal/limitation of life support as perceived by bedside nurses: a multicenter survey study.
We hypothesized that bedside nurses perceive significant variability in the pediatric intensivist thresholds for approaching a family about withdrawal/limitation of life-sustaining therapy. ⋯ Bedside pediatric intensive care unit nurses in this multicenter Canadian study perceive wide variability in intensivist thresholds for approaching a family to suggest withdrawal/limitation of life-sustaining therapy.