Bench-to-bedside review: Chloride in critical illness

ArticleinCritical care (London, England) 14(4):226 · July 2010with65 Reads
DOI: 10.1186/cc9052 · Source: PubMed
Chloride is the principal anion in the extracellular fluid and is the second main contributor to plasma tonicity. Its concentration is frequently abnormal in intensive care unit patients, often as a consequence of fluid therapy. Yet chloride has received less attention than any other ion in the critical care literature. New insights into its physiological roles have emerged together with progress in understanding the structures and functions of chloride channels. In clinical practice, interest in a physicochemical approach to acid-base physiology has directed renewed attention to chloride as a major determinant of acid-base status. It has also indirectly helped to generate interest in other possible effects of disorders of chloraemia. The present review summarizes key aspects of chloride physiology, including its channels, as well as the clinical relevance of disorders of chloraemia. The paper also highlights current knowledge on the impact of different types of intravenous fluids on chloride concentration and the potential effects of such changes on organ physiology. Finally, the review examines the potential intensive care unit practice implications of a better understanding of chloride.
    • "This was emphasised in an article written by Yunos et al. In 2010, when those authors searched PubMed for the term 'hyperchloraemia', it generated only 181 citations, while 'hypernatraemia' and 'hypercalcaemia' generated 2481 and 15,518 citations , respectively [22]. Searching the relevant literature related to AHF with hyponatraemia, we could not find results that included concentrations of chloride and their statistical interpretation. "
    [Show abstract] [Hide abstract] ABSTRACT: Aims: Heart failure (HF) is a major public health issue currently affecting more than 23 million patients worldwide. Hyponatraemia has been shown to be a predictor of poor outcome in patients with acute and chronic HF. Therefore, we aimed at finding a marker for early detection of patients at risk for developing hyponatraemia. To this end, the present study investigated the relationship between initial serum chloride and follow-up sodium levels in acute heart failure (AHF) patients. Methods and results: The present study was performed as a prospective, single-centre, observational research with a total of 152 hospitalised AHF patients. Compared to patients with initial normochloraemia, patients with initial hypochloraemia had a statistically significantly higher incidence of hyponatraemia after a 3-month follow-up [P<0.001; odds ratio (OR)=27.08, CI: 4.3-170.7]. A similar finding was obtained upon exclusion of patients with initial hyponatraemia with Fishers test [P=0.034; odds ratio (OR)=15.5, CI:1.7-140.6]. Binary logistic regression revealed a significantly increased in-hospital mortality in the hypochloraemic/normonatriaemic (OR=4.08, CI 1.08-15.43, P=0.039), but not in the hypochloraemic/hyponatraemic, normochloraemic/hyponatraemic or normonatriaemic/normochloraemic patients. Ejection fraction (EF) at admission was significantly higher in hypochloraemic/normonatriaemic, compared to normonatriaemic/normochloraemic patients, but similar to EF in both hypochloraemic/hyponatraemic and normochloraemic/hyponatraemic patients. The N-terminal precursor Brain Natriuretic Peptide (Nt-proBNP) levels at admission were significantly lower in hypochloraemic/normonatriaemic compared to hypochloraemic/hyponatraemic and normonatriaemic/normochloraemic patients, respectively. Conclusion: The data show that initial low serum chloride concentration is predictive of developing hyponatraemia and associated with increased in-hospital mortality in AHF patients.
    Full-text · Article · Mar 2016
    • "Indeed there is the increased risk of tissue oedema and deterioration in acid-base status and gas exchange [34]. There is also growing concern about the potential association between the use of chloriderich fluids and the development of a range of complications in critically ill patients including AKI, acidosis and coagulopathy [38, 39] . Indeed one of the hypotheses for the increased mortality seen in the patients receiving a fluid bolus in the FEAST study was the potential for hyperchloraemia to exacerbate the acid-base status and therefore vascular haemodynamics and myocardial performance [40]. "
    [Show abstract] [Hide abstract] ABSTRACT: Background: A conservative approach to fluid resuscitation improves survival in children with severe malaria; however, this strategy has not been formally evaluated in adults with the disease. Methods: Adults hospitalised with malaria at two tertiary referral hospitals in Myanmar received intravenous fluid replacement with isotonic saline, administered at a maintenance rate using a simple weight-based algorithm. Clinical and biochemical indices were followed sequentially. Results: Of 61 adults enrolled, 34 (56%) had Plasmodium falciparum mono-infection, 17 (28%) Plasmodium vivax mono-infection and 10 (16%) mixed infection; 27 (44%) patients were at high risk of death (P. falciparum infection and RCAM score ≥ 2). In the first six hours of hospitalisation patients received a mean 1.7 ml/kg/hour (range: 1.3-2.2) of intravenous fluid and were able to drink a mean of 0.8 ml/kg/hour (range: 0-3). Intravenous fluid administration and oral intake were similar for the remainder of the first 48 hours of hospitalisation. All 61 patients survived to discharge. No patient developed Adult Respiratory Distress Syndrome, a requirement for renal replacement therapy or hypotension (mean arterial pressure < 60mmHg). Plasma lactate was elevated (> 2 mmol/L) on enrolment in 26 (43%) patients but had declined by 6 hours in 25 (96%) and was declining at 24 hours in the other patient. Plasma creatinine was elevated (> 120 μmol/L) on enrolment in 17 (28%) patients, but was normal or falling in 16 (94%) at 48 hours and declining in the other patient by 72 hours. There was no clinically meaningful increase in plasma lactate or creatinine in any patient with a normal value on enrolment. Patients receiving fluid replacement with the conservative fluid replacement algorithm were more likely to survive than historical controls in the same hospitals who had received fluid replacement guided by clinical judgement in the year prior to the study (p = 0.03), despite having more severe disease (p < 0.001). Conclusions: A conservative fluid resuscitation strategy appears safe in adults hospitalised with malaria.
    Full-text · Article · Nov 2015
    • "Transport of chloride across cell membranes is facilitated by both voltage-gated and non-voltage-gated chloride channels [3]. Hyperchloremic metabolic acidosis, myocardial dysfunction, renal tubular defects and cystic fibrosis are among the many pathological conditions associated with disruption of chloride homeostasis [1,3,4]. The extensive literature on chloride physiology and pathophysiology is restricted mainly to assessing changes in extracellular fluid chloride levels or ion flux and largely neglects measurements of intracellular compartmental chloride concentrations. "
    [Show abstract] [Hide abstract] ABSTRACT: We recently reported that, in a concentration-dependent manner, chloride protects hepatic glutathione transferase zeta 1 from inactivation by dichloroacetate, an investigational drug used in treating various acquired and congenital metabolic diseases. Despite the importance of chloride ions in normal physiology, and decades of study of chloride transport across membranes, the literature lacks information on chloride concentrations in animal tissues other than blood. In this study we measured chloride concentrations in human liver samples from male and female donors aged 1 day to 84 years (n = 97). Because glutathione transferase zeta 1 is present in cytosol and, to a lesser extent, in mitochondria, we measured chloride in these fractions by high-performance liquid chromatography analysis following conversion of the free chloride to pentafluorobenzylchloride. We found that chloride concentration decreased with age in hepatic cytosol but increased in liver mitochondria. In addition, chloride concentrations in cytosol, (105.2 ± 62.4 mM; range: 24.7 - 365.7 mM) were strikingly higher than those in mitochondria (4.2 ± 3.8 mM; range 0.9 - 22.2 mM). These results suggest a possible explanation for clinical observations seen in patients treated with dichloroacetate, whereby children metabolize the drug more rapidly than adults following repeated doses, and also provide information that may influence our understanding of normal liver physiology. Copyright © 2015. Published by Elsevier Inc.
    Full-text · Article · Mar 2015
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