Contrast-associated acute kidney injury : does it really exist, and if so, what to do about it?

For decades, when contrast agents are administrated, physicians have been concerned because of the risk of inducing acute kidney injury (AKI). Recent literature questions the existence of AKI induced by contrast, but animal studies clearly showed harmful effects. The occurrence of contrast-associated AKI was likely overestimated in the past because of confounders for AKI. Several strategies have been investigated to reduce contrast-associated AKI but even for the most important one, hydration, there are conflicting data. Even if the occurrence rate of contrast-associated AKI is low, AKI is related to worse outcomes. Therefore, besides limiting contrast agent usage, general AKI preventive measurements should be applied in at-risk patients

AKI patients have worse long-term outcomes, especially in the immediate post-ICU period

Acute kidney injury (AKI) is associated with worse outcome in the acute phase of acute illness but also in the chronic phase. In a large Danish study in this issue of Critical Care, 1-year mortality was higher in patients with AKI than in patients without AKI. Mortality was most important during the first 50 days after admission to the intensive c are unit (ICU), whereas after 2 months the survival curves of patients with AKI and those of patients without AKI were similar. The reasons for this observation are not clear, but protracted critical illness and fragility after acute critical illness probably play important roles. Because we see more and more of these patients, they should be the focus of ICU research. Consequently, ICU and post-ICU care for these patients requires focus and a more integrated approach to the specific problems of these survivors of acute critical illness

Urinary chitinase 3-like protein 1 for early diagnosis of acute kidney injury : a prospective cohort study in adult critically ill patients

Background: Acute kidney injury (AKI) occurs frequently and adversely affects patient and kidney outcomes, especially when its severity increases from stage 1 to stages 2 or 3. Early interventions may counteract such deterioration, but this requires early detection. Our aim was to evaluate whether the novel renal damage biomarker urinary chitinase 3-like protein 1 (UCHI3L1) can detect AKI stage >= 2 more early than serum creatinine and urine output, using the respective Kidney Disease vertical bar Improving Global Outcomes (KDIGO) criteria for definition and classification of AKI, and compare this to urinary neutrophil gelatinase-associated lipocalin (UNGAL). Methods: This was a translational single-center, prospective cohort study at the 22-bed surgical and 14-bed medical intensive care units (ICU) of Ghent University Hospital. We enrolled 181 severely ill adult patients who did not yet have AKI stage >= 2 based on the KDIGO criteria at time of enrollment. The concentration of creatinine (serum, urine) and CHI3L1 (serum, urine) was measured at least daily, and urine output hourly, in the period from enrollment till ICU discharge with a maximum of 7 ICU-days. The concentration of UNGAL was measured at enrollment. The primary endpoint was the development of AKI stage >= 2 within 12 h after enrollment. Results: After enrollment, 21 (12 %) patients developed AKI stage >= 2 within the next 7 days, with 6 (3 %) of them reaching this condition within the first 12 h. The enrollment concentration of UCHI3L1 predicted the occurrence of AKI stage >= 2 within the next 12 h with a good AUC-ROC of 0.792 (95 % CI: 0.726-0.849). This performance was similar to that of UNGAL (AUC-ROC of 0.748 (95 % CI: 0.678-0.810)). Also, the samples collected in the 24-h time frame preceding diagnosis of the 1st episode of AKI stage >= 2 had a 2.0 times higher (95 % CI: 1.3-3.1) estimated marginal mean of UCHI3L1 than controls. We further found that increasing UCHI3L1 concentrations were associated with increasing AKI severity. Conclusions: In this pilot study we found that UCHI3L1 was a good biomarker for prediction of AKI stage >= 2 in adult ICU patients

Abdominal decompression for abdominal compartment syndrome in critically ill patients: a retrospective study

Background. The abdominal compartment syndrome (ACS) refers to organ dysfunction that may occur as a result of increased intra-abdominal pressure (IAP). Successful management may require abdominal decompression and temporary abdominal closure (TAC). The aim of this study was to analyze the characteristics of patients requiring abdominal decompression, to describe the methods used for TAC, and to study the outcome of these patients. Methods. A series of critically ill patients who required abdominal decompression for ACS between January 2000 and March 2007 were reviewed retrospectively. Age, gender, severity of organ dysfunction before decompression and the cause of ACS as well as the type of abdominal closure system and length of ICU-stay were recorded. Definitive abdominal closure and in-hospital mortality were the main outcome parameters. Results. Eighteen patients with primary ACS and 6 with secondary ACS required decompressive laparotomy. Patients ages ranged from 18 to 89 years (mean 50.7). The median preoperative IAP was 26mmHg, and IAP decreased to 13mmHg after decompressive laparotomy. Organ function, as quantified by the SOFA scoring system, improved significantly after the intervention. Eight patients had immediate primary fascial closure after the decompressive procedure and 16 patients required TAC. The majority of the survivors underwent planned ventral hernia repair at a later stage. The mean length of stay in the ICU was 23 (+/- 16) days. Overall, fifteen patients survived (63%). Conclusions. Decompressive laparotomy was effective in reducing IAP and was associated with an improvement in organ function. In most of the patients, the abdomen could not be closed after decompression, and fascial repair was delayed

Outcome following burns from 1985 to 2004 in the centre for severely burned patients, Ghent University Hosptial, Belgium

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Paving the way for precision medicine v2.0 in intensive care by profiling necroinflammation in biofluids

Current clinical diagnosis is typically based on a combination of approaches including clinical examination of the patient, clinical experience, physiologic and/or genetic parameters, high-tech diagnostic medical imaging, and an extended list of laboratory values mostly determined in biofluids such as blood and urine. One could consider this as precision medicine v1.0. However, recent advances in technology and better understanding of molecular mechanisms underlying disease will allow us to better characterize patients in the future. These improvements will enable us to distinguish patients who have similar clinical presentations but different cellular and molecular responses. Treatments will be able to be chosen more "precisely", resulting in more appropriate therapy, precision medicine v2.0. In this review, we will reflect on the potential added value of recent advances in technology and a better molecular understanding of necrosis and inflammation for improving diagnosis and treatment of critically ill patients. We give a brief overview on the mutual interplay between necrosis and inflammation, which are two crucial detrimental factors in organ and/or systemic dysfunction. One of the challenges for the future will thus be the cellular and molecular profiling of necroinflammation in biofluids. The huge amount of data generated by profiling biomolecules and single cells through, for example, different omic-approaches is needed for data mining methods to allow patient-clustering and identify novel biomarkers. The real-time monitoring of biomarkers will allow continuous (re)evaluation of treatment strategies using machine learning models. Ultimately, we may be able to offer precision therapies specifically designed to target the molecular set-up of an individual patient, as has begun to be done in cancer therapeutics

Semicontinuous intra-abdominal pressure measurement using an intragastric Compliance catheter

OBJECTIVE: To compare intra-abdominal pressure (IAP) measurements obtained from an intragastric Compliance catheter with the pressure measured directly in the abdominal cavity. DESIGN AND SETTING: Prospective cohort study in an operating room of the Ghent University Hospital PATIENTS: Seven patients undergoing elective laparoscopic cholecystectomy. INTERVENTIONS: IAP was obtained from both an intragastric catheter and directly from the peritoneal cavity at 1-minute intervals in patients undergoing elective cholecystectomy and compared using Bland-Altman analysis. MEASUREMENTS AND RESULTS: In 156 paired measurements obtained from 7 patients the mean difference between IAPgastric and IAPref was 0.12+/-0.70 mmHg (95% CI 0.01-0.23). CONCLUSIONS: IAP measured using an intragastric Compliance catheter reliably reflects the reference IAP in patients undergoing laparoscopic cholecystectomy