Critical care : the official journal of the Critical Care Forum
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Comment Letter
Prophylactic open abdomen in patients with postoperative intra-abdominal hypertension.
Postoperative intra-abdominal hypertension (IAH) is a frequent occurrence in critically ill patients operated on for severe abdominal trauma, secondary peritonitis or ruptured abdominal aortic aneurysm. IAH may progress to abdominal compartment syndrome (ACS) with new-onset organ dysfunction. Early recognition of IAH and interventions that prevent the development of ACS may preserve vital organ functions and increase the probability of survival. ⋯ Because significant morbidity and mortality are associated with the open abdomen, the measurement of IAP immediately after the fascial closure, when feasible, could offer an objective method for determining the optimal IAP threshold for leaving the abdomen open. The management of the open abdomen requires a temporary abdominal closure (TAC) system that would ideally prevent the development of ACS and facilitate later primary fascia closure. Among several TAC systems, the most promising are those that provide negative pressure to the wound or continuous fascial traction or both.
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The early application of fibrinogen could potentially reverse haemodilution-induced coagulopathy, although the impact of varying concentrations of fibrinogen to reverse dilutional coagulopathy has not been studied in vivo. We postulated that fibrinogen concentration is correlated with blood loss in a pig model of coagulopathy with blunt liver injury. ⋯ Restoring fibrinogen with 70 or 200 mg kg-1 after severe dilutional coagulopathy safely improved coagulation and attenuated blood loss after experimental blunt liver trauma. The higher dosage of fibrinogen was not associated with a further reduction in blood loss.
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Certain noble gases, though inert, exhibit remarkable biological properties. Notably, xenon and argon provide neuroprotection in animal models of central nervous system injury. ⋯ Their data are of interest as argon is more abundant, and therefore cheaper, than xenon (the latter of which is currently in clinical trials for perinatal hypoxic-ischemic brain injury; TOBYXe; NCT00934700). We eagerly await in vivo data to complement the promising in vitro data hailing argon neuroprotection.
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Mechanical ventilation (MV) can injure the lungs and contribute to an overwhelming inflammatory response, leading to acute renal failure (ARF). We previously showed that poly(adenosine diphosphate-ribose) polymerase (PARP) is involved in the development of ventilator-induced lung injury (VILI) and the related ARF, but the mechanisms underneath remain unclear. In the current study we therefore tested the hypothesis that renal blood flow and endothelial, functional and tissue changes in the kidney of rats with lipopolysaccharide (LPS)-induced lung injury aggravated by MV, is caused, in part, by activation of PARP by peroxynitrite. ⋯ The peroxynitrite-induced PARP activation is involved in renal hypoperfusion, impaired endothelium-dependent vasodilation and resultant dysfunction, and injury, in a model of lung injury.
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In a recent issue of Critical Care, Brandt and colleagues report the effects of a 'liberal' fluid loading protocol compared to a more 'restrictive' protocol on hemodynamics and mortality in pigs in which septic shock had been induced. It appears that the former protocol was associated with higher mortality in spite of improved hemodynamics compared to the latter. ⋯ They also do not exclude a specific toxic effect of the larger volumes of hydroxyethyl starch in the 'liberal' strategy. The precise nature of a toxic effect remains obscure, however, but may involve the kidneys.