Hyperchloraemia is associated with acute kidney injury and mortality in the critically ill: A retrospective observational study in a multidisciplinary intensive care unit.

PURPOSE: The aim of this study was to determine whether serum chloride and changes in serum chloride over time were associated with acute kidney injury (AKI) or intensive care unit (ICU) mortality in a heterogenous critically ill population. MATERIALS AND METHODS: The study was a retrospective observational study of 250 adult patients admitted to a multidisciplinary academic ICU. Serum chloride within 48 h of admission, changes in chloride, and other biochemical and clinical parameters were evaluated as predictors of AKI and mortality. RESULTS: Hyperchloraemia occurred in 143 (57.2%) patients within 48 h of ICU admission. Hyperchloraemia at 48 h was significantly associated with AKI, OR = 6.44 (95% CI 2.95-14.10) and mortality, OR = 2.46 (95% CI 1.22-4.94) on univariate analysis, with this association persisting on multivariable analysis. An increase in serum chloride was also associated with a significantly increased risk of AKI and mortality on univariate analysis. Hyperchloraemia on admission was, however, not associated with AKI or death. Of the 150 patients with AKI, 147 (98.0%) had developed AKI by 48 h. CONCLUSIONS: Hyperchloraemia and increasing serum chloride are associated with adverse outcomes in critically ill patients. There is equipoise as to whether this represents an association, an epiphenomenon or causation.

Serum procalcitonin levels predict acute kidney injury in critically ill patients.

AIM: To determine whether admission procalcitonin (PCT) was associated with the subsequent development of acute kidney injury (AKI) in a general population of critically ill patients. METHODS: The study was a retrospective observational study conducted in a multidisciplinary intensive care unit (ICU) over a period of 1 year. Adult patients who had a PCT performed on admission and who did not have chronic kidney disease (CKD) or AKI on admission, were evaluated for the development of AKI within the first week of ICU admission, according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria. The association between PCT on admission and the development of AKI was explored for the entire cohort and for septic and non-septic subgroups. RESULTS: Two hundred and one patients were included in the study. The incidence of AKI in the first 7 days of ICU admission was 36.8%. PCT, age, the presence of shock on admission, and sepsis were significantly associated with AKI on univariate analysis. Multivariable analysis of the entire cohort revealed that age, shock and sepsis remained independent predictors of AKI, while PCT was no longer significant. When the septic and non-septic patients were analyzed separately a PCT ≥10 ng/mL remained the only significant predictor of AKI in the non-septic patients (OR 4.430; 95% CI 1.464-13.399), but was not an independent predictor of AKI in septic patients. CONCLUSION: The main finding of this study was the significant association of an elevated PCT on admission with the development of AKI in the non-septic patient. An elevated PCT in a non-septic patient identifies a patient at increased risk of AKI. PCT requires further study as a novel biomarker of AKI in non-septic patients.

Ventricular septal defect following blunt chest trauma.

We present a 32-year-old male with ventricular septal defect (VSD) following blunt chest trauma. Traumatic VSD is a rare but potentially life-threatening injury, the severity, course and presentation of which are variable. While the diagnosis of myocardial injury may be challenging, cardiac troponins are useful as a screening and diagnostic test. The proposed pathophysiological mechanisms in the development of traumatic VSD are early mechanical rupture and delayed inflammatory rupture. We conducted a literature review to investigate the pathogenesis, distribution of patterns of presentation, and the associated prognoses in patients with VSD following blunt chest trauma. We found that traumatic VSDs diagnosed within 48 hours were more likely to be severe, require emergency surgery and were associated with a higher mortality. Children with traumatic VSDs had an increased mortality risk. Smaller lesions may be managed conservatively but should be followed up to detect late complications. In both groups elective repair was associated with a good outcome.