Serum osmolality and outcome in intensive care unit patients

Holtfreter, Birte; Bandt, Christoph; Kuhn, Sven–Olaf; Grunwald, U.; Lehmann, Christian; Schutt, Christopher A.; Gründling, Matthias

doi:10.1111/j.1399-6576.2006.01096.x

Cited by 44 publications

(33 citation statements)

References 47 publications

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“…Hyperosmolality is related to illness severity [23] and has been described as a risk factor for critical illness neuropathy [24]. It is worth noting that the study by Garnacho-Montero and colleagues [24] did not differentiate between myopathy and neuropathy.…”

Section: Discussionmentioning

confidence: 99%

Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study

et al. 2010

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IntroductionNon-excitable muscle membrane indicates critical illness myopathy (CIM) during early critical illness. We investigated predisposing risk factors for non-excitable muscle membrane at onset of critical illness.MethodsWe performed sequential measurements of muscle membrane excitability after direct muscle stimulation (dmCMAP) in 40 intensive care unit (ICU) patients selected upon a simplified acute physiology (SAPS-II) score ≥ 20 on 3 successive days within 1 week after ICU admission. We then investigated predisposing risk factors, including the insulin-like growth factor (IGF)-system, inflammatory, metabolic and hemodynamic parameters, as well as suspected medical treatment prior to first occurrence of abnormal dmCMAP. Nonparametric analysis of two-factorial longitudinal data and multivariate analysis were used for statistical analysis.Results22 patients showed abnormal muscle membrane excitability during direct muscle stimulation within 7 (5 to 9.25) days after ICU admission. Significant risk factors for the development of impaired muscle membrane excitability in univariate analysis included inflammation, disease severity, catecholamine and sedation requirements, as well as IGF binding protein-1 (IGFBP-I), but did not include either adjunctive hydrocortisone treatment in septic shock, nor administration of neuromuscular blocking agents or aminoglycosides. In multivariate Cox regression analysis, interleukin-6 remained the significant risk factor for the development of impaired muscle membrane excitability (HR 1.006, 95%-CI (1.002 to 1.011), P = 0.002).ConclusionsSystemic inflammation during early critical illness was found to be the main risk factor for development of CIM during early critical illness. Inflammation-induced impairment of growth-factor mediated insulin sensitivity may be involved in the development of CIM.

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Section: Discussionmentioning

confidence: 99%

Risk factors in critical illness myopathy during the early course of critical illness: a prospective observational study

et al. 2010

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“…Several common disorders are known (or thought) to be caused by perturbations in fluid osmolarity. Tissue burns, dehydration, heat stroke, diabetes mellitus, diabetes insipidus, hypernatremia, and uremia are all associated with elevated extracellular osmolarity (11, 96–99). Extracellular fluid hyperosmolarity is also believed to play an inflammatory role in asthma and cystic fibrosis (11).…”

Section: Extracellular Hypertonicity As An Inflammatory Stimulusmentioning

confidence: 99%

The role of hyperosmotic stress in inflammation and disease

Brocker

Thompson²,

Vasiliou

2012

BioMolecular Concepts

236

212

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Hyperosmotic stress is an often overlooked process that potentially contributes to a number of human diseases. Whereas renal hyperosmolarity is a well-studied phenomenon, recent research provides evidence that many non-renal tissues routinely experience hyperosmotic stress that may contribute significantly to disease initiation and progression. Moreover, a growing body of evidence implicates hyperosmotic stress as a potent inflammatory stimulus by triggering proinflammatory cytokine release and inflammation. Under physiological conditions, the urine concentrating mechanism within the inner medullary region of the mammalian kidney exposes cells to high extracellular osmolarity. As such, renal cells have developed many adaptive strategies to compensate for increased osmolarity. Hyperosmotic stress is linked to many maladies, including acute and chronic, as well as local and systemic, inflammatory disorders. Hyperosmolarity triggers cell shrinkage, oxidative stress, protein carbonylation, mitochondrial depolarization, DNA damage, and cell cycle arrest, thus rendering cells susceptible to apoptosis. However, many adaptive mechanisms exist to counter the deleterious effects of hyperosmotic stress, including cytoskeletal rearrangement and up-regulation of antioxidant enzymes, transporters, and heat shock proteins. Osmolyte synthesis is also up-regulated and many of these compounds have been shown to reduce inflammation. The cytoprotective mechanisms and associated regulatory pathways that accompany the renal response to hyperosmolarity are found in many non-renal tissues, suggesting cells are commonly confronted with hyperosmotic conditions. Osmoadaptation allows cells to survive and function under potentially cytotoxic conditions. This review covers the pathological consequences of hyperosmotic stress in relation to disease and emphasizes the importance of considering hyperosmolarity in inflammation and disease progression.

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“…Others have reported on the use of the score in combination with other well-known predictive scores, such as the Acute Physiology and Chronic Health Evaluation (APACHE) II [11] or the Simplified Acute Physiology Score II (SAPS) [12]. Aside from these efforts to evaluate its performance, the SOFA score has been compared with other scores commonly used in the ICU to predict mortality such as APACHE II [2,13,14], SAPS II [15], the Multiple Organ Dysfunction Score [2,16], or the Logistic Organ Dysfunction System [17,18].…”

Section: Introductionmentioning

confidence: 99%