Critical care : the official journal of the Critical Care Forum
-
A recent observational study in a large cohort of critically ill patients confirms the association between hyperlactatemia and mortality. The mechanisms regulating the rates of lactate production and clearance in critical illness remain poorly understood. ⋯ Possible mechanisms include regional hypoperfusion, an inflammation-induced upregulation of the glycolitic flux, alterations in lactate-clearing mechanisms, and increases in the work of breathing. Understanding how these complex processes interact to produce elevations in lactate continues to be an important area of research.
-
The review article by Xie and colleagues examines the impact of noise and noise reduction strategies on sleep quality for critically ill patients. Evaluating the impact of noise on sleep quality is challenging, as it must be measured relative to other factors that may be more or less disruptive to patients' sleep. ⋯ Furthermore, most research in this field has focused on noise level, whereas acousticians typically evaluate additional parameters such as noise spectrum and reverberation time. The authors highlight the disparate results and limitations of existing studies, including the lack of attention to other acoustic parameters besides sound level, and the combined effects of different sleep disturbing factors.
-
Acetaminophen (APAP) toxicity is the most common cause of acute liver failure in the US and Europe. Massive hepatocyte necrosis is the predominant feature of APAP-induced acute liver injury (ALI). Liver regeneration is a vital process for survival after a toxic insult, it occurs at a relative late time point after the injurious phase. Currently, N-acetylcysteine (NAC), a glutathione precursor, is the antidote for acetaminophen overdose. However, NAC is effective only for patients who present within hours of an acute overdose, and is less effective for late-presenting patients. It is possible that in delayed patients, previously reduced endogenous glutathione (GSH) level has restored and prolonged treatment with NAC might be toxic and impair liver regeneration. Therefore, we hypothesize that prolonged treatment with NAC impairs liver regeneration in ALI induced by APAP. ⋯ Prolonged treatment with NAC impairs liver regeneration in ALI induced by APAP.
-
Advanced glycation endproducts (AGEs) are primarily known as a complication in diabetic patients through their mediation of the inflammatory response. However, a variety of studies have demonstrated enhanced formation of AGEs in cardiovascular disorders. Despite the large number of AGEs produced during the Maillard reaction, recent focus is on the major non-crosslinking AGE Nepsilon-carboxymethyllysine. ⋯ Therefore, AGEs may participate in the inflammatory response related to cardiac dysfunction in critically ill patients. Moreover, life-saving ventilation stimulates AGE formation in these patients. This interesting study raises the question of whether AGEs in critically ill patients are a driving force of the disease.