Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Observational Study
Enterocyte Damage: A Piece in the Puzzle of Post Cardiac Arrest Syndrome.
Cardiac arrest is considered to be a cause of small bowel ischemia, but the consequences of cardiac arrest on the human small bowel have been rarely studied. Plasma citrulline concentration is a marker of functional enterocyte mass, and plasma intestinal fatty acid-binding protein (I-FABP) concentration is a marker of enterocyte damage. We aimed to measure enterocyte biomarkers after cardiac arrest and to study the prognostic value of biomarker abnormalities. ⋯ Cardiac arrest resuscitation is associated with evidence of small bowel mucosal damage in most patients, with a short and intense I-FABP elevation at admission and a decrease in citrulline concentration during the first day. In this study, low plasma citrulline and high I-FABP concentrations at ICU admission were predictive of a poor neurological outcome. This study confirms that cardiac arrest is a model of small bowel mucosal ischemia and suggests that enterocyte damage is a piece in the puzzle of post-cardiac arrest syndrome.
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Muscle loss accompanies severe burn; in this hyper-catabolic state, muscle undergoes atrophy through protein degradation and disuse. Muscle volume is related to the relative rates of cellular degradation and myogenesis. We hypothesize that muscle atrophy after injury is in part because of insufficient myogenesis associated with the hyper-inflammatory response. ⋯ We showed that severe burn induces both increased cell death and proliferation. Myogenesis, however, does not counterbalance increased cell death after burn. Data suggest insufficient myogenesis might be associated with pro-inflammatory mediator TNF activity.
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Acute alterations in skeletal muscle protein metabolism are a well-established event associated with the stress response to burns. Nevertheless, the long-lasting effects of burn injury on skeletal muscle protein turnover are incompletely understood. This study was undertaken to investigate fractional synthesis (FSR) and breakdown (FBR) rates of protein in skeletal muscle of pediatric burn patients (n = 42, >30% total body surface area burns) for up to 1 year after injury. ⋯ Therefore, net protein balance was lower in burn patients compared with healthy men from 2 weeks to 12 months post-injury (P < 0.05). These findings show that skeletal muscle protein turnover stays elevated for up to 1 year after burn, an effect attributable to simultaneous increases in FBR and FSR. Muscle FBR exceeds FSR during this time, producing a persistent negative net protein balance, even in the post-prandial state, which likely contributes to the prolonged cachexia seen in burned victims.
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Patients with severe hypernatremia who receive conventional treatment are often undertreated. Data on the management of acute hypernatremia using continuous venovenous hemofiltration (CVVH) are limited to anecdotes. This study aimed to evaluate the efficacy and safety of CVVH treatment for acute severe hypernatremia in critically ill patients in a retrospective cohort. ⋯ The CVVH group had a significantly greater reduction in the serum sodium concentration (0.78 [0.63-1.0] mmol/L/h versus 0.13 [0.009-0.33] mmol/L/h), P < 0.001) and an improved 28-day survival rate (34.8% vs. 8.7%, P = 0.002) compared with the conventional treatment group. The two groups did not differ significantly in treatment-related complications. CVVH treatment is possibly more effective than conventional treatment for the management of acute severe hypernatremia in critically ill patients.
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In acute kidney injury (AKI), fluid accumulation is associated with poor outcome. We aimed to determine whether fluid intake or output had the major role. ⋯ Increased fluid intake in early AKI was an independent risk factor for AKI III.