Critical care : the official journal of the Critical Care Forum
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Traumatic cardiac arrest resuscitation is considered a heroic and futile endeavor. However, newer articles have more promising statistics and divide between prehospital ground and helicopter transport. Here we discuss why there might be a difference in the survivability of this subset of trauma patients.
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Timing of therapy plays a pivotal role in intensive care patients. Although being evident and self-explanatory, it has to be considered that the appropriateness of a specific therapeutic intervention is likewise important. In view of antibiotic therapy of critically ill patients, the available evidence supports the concept of hitting hard, early (as soon as possible and at least before the onset of shock) and appropriately. ⋯ The right dose and timing for renal replacement therapy is still discussed controversially and remains a subjective decision of the attending physician. New renal biomarkers may perhaps be helpful to validate when (and how) renal replacement therapy should be performed best. Last but not least, all therapeutic interventions should take the individual co-morbidities and underlying pathophysiological conditions into account.
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Editorial Comment Review
Diaphragmatic dysfunction in the intensive care unit: caught in the cross-fire between sepsis and mechanical ventilation.
Accumulating evidence indicates that diaphragmatic weakness is common and frequently severe in mechanically ventilated patients. Supinski and Callahan now report that infection is a major risk factor for diaphragmatic weakness in this patient population. ⋯ Mechanical ventilation itself has also been found to induce diaphragmatic weakness along with cellular changes resembling those found in sepsis. Future studies should be directed at understanding the interaction between sepsis and mechanical ventilation, and to developing therapeutic approaches that target their common cellular pathways implicated in diaphragmatic weakness.
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Bacterial sepsis and septic shock are complex inflammatory disorders associated with a systemic inflammatory response syndrome. In the most severe cases of infection, an overzealous release of pro-inflammatory cytokines and inflammatory mediators by activated leukocytes, epithelial cells and endothelial cells, known as a 'cytokine storm', leads to deleterious effects such as organ dysfunction and even death. By the end of the 20th century, natural killer (NK) cells were for the first time identified as important players during sepsis. ⋯ Bacterial sensors (such as Toll-like receptors) have recently been shown to be expressed at the protein level in these cells. In addition, NK cells are important sources of interferon-γ and granulocyte-macrophage colony-stimulating factor, which are pro-inflammatory cytokines necessary to fight infection but can contribute to deleterious inflammation as well. Interestingly, an adaptative response occurs aimed to silence them, similar to the well-known phenomenon of endotoxin reprogramming.
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The greatest advances in critical care over the past two decades have been achieved through doing less to the patient. We have learnt through salutary experience that our burgeoning Master-of-the-Universe capabilities and the oh-so-obvious stratagems instilled in us from youth were often ineffective or even deleterious. This re-education process, however, is far from complete. ⋯ We need to improve trial design in the heterogeneous populations we treat, and to move away from syndromic fixations that, while offering convenience, have generally proved counterproductive. Importantly, we need to discover a far more holistic approach to patient care, evolving from the prevailing overmedicalized, number-crunching perspective towards a true multidisciplinary effort that embraces psychological as well as physiological well-being, with appropriate pharmacological minimization or supplementation. Complacency, with an unfair apportion of blame on the patient for not getting better, is the biggest threat to continued improvement.