The Development of Intensive Care Unit Acquired Hypernatremia Is Not Explained by Sodium Overload or Water Deficit: A Retrospective Cohort Study on Water Balance and Sodium Handling.

Background. ICU acquired hypernatremia (IAH, serum sodium concentration (sNa) ≥ 143 mmol/L) is mainly considered iatrogenic, induced by sodium overload and water deficit. Main goal of the current paper was to answer the following questions: Can the development of IAH indeed be explained by sodium intake and water balance? Or can it be explained by renal cation excretion? Methods. Two retrospective studies were conducted: a balance study in 97 ICU patients with and without IAH and a survey on renal cation excretion in 115 patients with IAH. Results. Sodium intake within the first 48 hours of ICU admission was 12.5 [9.3-17.5] g in patients without IAH (n = 50) and 15.8 [9-21.9] g in patients with IAH (n = 47), p = 0.13. Fluid balance was 2.3 [1-3.7] L and 2.5 [0.8-4.2] L, respectively, p = 0.77. Urine cation excretion (urine Na + K) was < sNa in 99 out of 115 patients with IAH. Severity of illness was the only independent variable predicting development of IAH and low cation excretion, respectively. Conclusion. IAH is not explained by sodium intake or fluid balance. Patients with IAH are characterized by low urine cation excretion, despite positive fluid balances. The current paradigm does not seem to explain IAH to the full extent and warrants further studies on sodium handling in ICU patients.

Microcirculatory perfusion derangements during continuous hemofiltration with fixed dose of ultrafiltration in stabilized intensive care unit patients.

INTRODUCTION: Acute kidney injury (AKI) is a well-known complication in critically ill patients. Little is known about the timing and the ultrafiltration dose after initial resuscitation. In vivo microscopy of the microcirculation has been suggested as alternative for the assessment of volume status. Previous studies contribute to the understanding that intravascular hypovolemia is reflected by microcirculatory blood flow changes not detected by conventional methods. The aim of our study was to assess microcirculatory blood flow changes during negative fluid balance ultrafiltration in patients with oliguric AKI. MATERIALS AND METHODS: Patients with oliguric AKI on renal replacement therapy were included after hemodynamic stabilization. Target was a predefined negative fluid balance; subsequently, a stepwise decrease in amount of substitution fluid was achieved. The data were recorded at baseline and after each change. RESULTS: Fifteen patients were included in the study. Microcirculatory blood flow index did not change significantly between baseline and endpoint (2.90 [2.87-3.00] vs 2.90 [2.75-3.00], P=.57). During treatment, heart rate decreased from 96 (80-111) to 94 (79-110) beats per minute (P=.01), without a significant change in mean arterial blood pressure (80 [68-95 mm Hg] vs 79 [65-91 mm Hg], P=.5). CONCLUSION: Microcirculatory blood flow is not altered by reduced substitution during renal replacement therapy.

The epidemiology of intra-abdominal flora in critically ill patients with secondary and tertiary abdominal sepsis.

BACKGROUND: Background: Different micro-organisms can be cultured from abdominal fluid obtained from patients with intra-abdominal infection resulting from a perforated digestive tract. We evaluated a cohort of patients with abdominal sepsis admitted to the intensive care with the aim of obtaining more insight into the type of microorganisms involved and the efficacy of treatment. MATERIALS AND METHODS: A 5-year prospective observational cohort study was performed in patients admitted to the intensive care unit with abdominal sepsis syndrome, defined as a perforation of the digestive tract and inflammatory response with organ failure. Abdominal fluid was obtained for microbial culture during the surgical procedures and from abdominal drains. The initial treatment protocol was cefotaxim, ciprofloxacin, metronidazole, and amphotericin B, tailored according to microbiological results. Selective decontamination of the digestive tract was administered to prevent secondary endogenous infections. RESULTS: Abdominal fluid was taken for microbial culture from 221 of the 239 patients admitted with abdominal sepsis. Aerobic Gram-negative bacteria (AGNB) were found in 52.9% of the cultures of abdominal fluid taken at the time of operation, of which 45% were Escherichia coli; in 36% of patients more than one AGNB was found. The incidence of AGNB was highest in colorectal perforations (68.6%) and perforated appendicitis (77.8%) and lowest in gastroduodenal perforations (20.5%). Gram-positive bacteria were found in 42.5% of the abdominal fluid cultures and most frequently in colorectal perforations (50.0%). Candida was found in 19.9% of patients, with 59.1% of these cultures being Candida albicans. The incidence of Candida was 41.0% in gastroduodenal perforations and 11.8% in colorectal perforation. Anaerobic bacteria were cultured in 77.8% of patients with perforated appendicitis. Over time, the prevalence of AGNB in abdominal fluid decreased from 117 patients (52.9%) in the first culture to one patient (6.7%) in week 4 (efficacy 87%). The prevalence of Gram-positive bacteria increased from 42.5% to 86.7% in a 4-week period. CONCLUSION: The composition of the intra-abdominal flora found in critically ill patients with abdominal sepsis varies depending on the location of the perforation. The efficacy of combined surgical and antibiotic treatment was 87% in 4 weeks for AGNB.

Safety of citrate based hemofiltration in critically ill patients at high risk for bleeding: a comparison with nadroparin.

PURPOSE: To study the incidence and severity of bleeding in high risk critically ill patients during high volume, citrate based continuous veno-venous hemofiltration (CVVH). DESIGN: A prospective 1-year observational cohort study comparing citrate based CVVH with nadroparin based CVVH. PROCEDURES: Critically ill patients with multiple organ dysfunction and in need of CVVH were observed for bleeding complications during their CVVH sessions. Pre-defined criteria determined that patients were treated with citrate based CVVH in case of active bleeding or increased risk for bleeding. Otherwise nadroparin was used as anticoagulant. Statistical and outcome methods: The incidence of bleeding complications, the number of transfused blood cell concentrates and the filter-run-time were recorded. Analyses were made by non-parametric tests. MAIN FINDINGS: Fifty-five patients received 272 CVVH sessions. In the citrate group 14.8% experienced a bleeding complication compared to 25% in the nadroparin group (p=0.04). The number of transfused red blood cell concentrates was not different between groups. The nadroparin group had a longer filter run time (median 31.5 hours versus 22.5 hours, p=0.0001). CONCLUSIONS: In high risk critically ill patients citrate based anticoagulation for CVVH is safe in terms of bleeding complications and transfusion requirements.

Filter run time in CVVH: pre- versus post-dilution and nadroparin versus regional heparin-protamine anticoagulation.

BACKGROUND/AIMS: To study the effect of different modes of continuous veno-venous haemofiltration (CVVH) on filter run time (FRT). METHODS: We studied, in two consecutive prospective, randomised and crossover studies, 16 and 15 patients with acute renal failure during critical illness. Study A compared pre- versus post-dilution, and study B compared regional anticoagulation with heparin (pre-filter) and protamine (post-filter) (HP) versus nadroparin (NP) pre-filter. All CVVH sessions were standardised. Analyses were by Wilcoxon rank sum tests. RESULTS: Study A: During pre-dilution the median FRT was 45.7 vs. 16.1 h in post-dilution CVVH (p = 0.005). The median creatinine clearance during pre-dilution was 33 vs. 45 ml/min in post-dilution (p = 0.001). Study B: During NP, median FRT was 39.5 vs. 12.3 h during HP CVVH (p = 0.045). CONCLUSIONS: Pre-dilution CVVH results in the greatest FRT but a lower plasma creatinine clearance compared to post-dilution. Regional anticoagulation with heparin-protamine resulted in a significantly shorter FRT compared to systemic NP anticoagulation.

Acute cardiorespiratory failure as presenting symptom of chronic lymphocytic leukemia.

A patient with acute cardiorespiratory failure caused by hyperleukocytosis due to chronic lymphocytic leukaemia (CLL) is described. Although acute pulmonary failure due to leukostasis is a known and often postmortem finding in patients with acute myelocytic leukaemia (AML) or chronic myelocytic leukaemia (CML) in blastic crises, it is rare in CLL.