H.M. Oudemans-van Straaten
VU University Medical Center
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Publication
Featured researches published by H.M. Oudemans-van Straaten.
Journal of Critical Care | 2015
S. Rijkenberg; W. Stilma; Henrik Endeman; Robert-Jan Bosman; H.M. Oudemans-van Straaten
PURPOSE The Behavioral Pain Scale (BPS) and Critical-Care Pain Observation Tool (CPOT) are behavioral pain assessment tools for uncommunicative and sedated intensive care unit (ICU) patients. This study compares the discriminant validation and reliability of the CPOT and the BPS, simultaneously, in mechanically ventilated patients on a mixed-adult ICU. MATERIALS AND METHODS This is a prospective observational cohort study in 68 mechanically ventilated medical ICU patients who were unable to report pain. RESULTS The BPS and CPOT scores showed a significant increase of 2 points between rest and the painful procedure (turning). The median BPS scores between rest and the nonpainful procedure (oral care) showed a significant increase of 1 point, whereas the median CPOT score remained unchanged. The interrater reliability of the BPS and CPOT scores showed a fair to good agreement (0.74 and 0.75, respectively). CONCLUSIONS This study showed that the BPS and the CPOT are reliable and valid for use in a daily clinical setting. Although both scores increased with a presumed painful stimulus, the discriminant validation of the BPS use was less supported because it increased during a nonpainful stimulus. The CPOT appears preferable in this particular group of patients, especially with regard to its discriminant validation.
Intensive Care Medicine | 2017
Lui G. Forni; Michael Darmon; Marlies Ostermann; H.M. Oudemans-van Straaten; Ville Pettilä; John R. Prowle; Miet Schetz; Michael Joannidis
Acute kidney injury (AKI) is a frequent complication of critical illness and carries a significant risk of short- and long-term mortality, chronic kidney disease (CKD) and cardiovascular events. The degree of renal recovery from AKI may substantially affect these long-term endpoints. Therefore maximising recovery of renal function should be the goal of any AKI prevention and treatment strategy. Defining renal recovery is far from straightforward due in part to the limitations of the tests available to assess renal function. Here, we discuss common pitfalls in the evaluation of renal recovery and provide suggestions for improved assessment in the future. We review the epidemiology of renal recovery and of the association between AKI and the development of CKD. Finally, we stress the importance of post-discharge follow-up of AKI patients and make suggestions for its incorporation into clinical practice. Summary key points are that risk factors for non-recovery of AKI are age, CKD, comorbidity, higher severity of AKI and acute disease scores. Second, AKI and CKD are mutually related and seem to have a common denominator. Third, despite its limitations full recovery of AKI may best be defined as the absence of AKI criteria, and partial recovery as a fall in AKI stage. Fourth, after an episode of AKI, serial follow-up measurements of serum creatinine and proteinuria are warranted to diagnose renal impairment and prevent further progression. Measures to promote recovery are similar to those preventing renal harm. Specific interventions promoting repair are still experimental.
Journal of Critical Care | 2017
E.M.J. Durlinger; A.M.E. Spoelstra-de Man; Bob Smit; H. J. de Grooth; Armand Rj Girbes; H.M. Oudemans-van Straaten; Yvo M. Smulders
Background: Concerns have been expressed regarding a possible association between arterial hyperoxia and adverse outcomes in critically ill patients. Oxygen status is commonly monitored noninvasively by peripheral saturation monitoring (SpO2). However, the risk of hyperoxia above specific SpO2 levels in critically ill patients is unknown. The purpose of this study was to determine a threshold value of SpO2 above which the prevalence of arterial hyperoxia distinctly increases. Methods: This is a cross‐sectional study in adult mechanically ventilated intensive care patients in a tertiary referral center. In 100 patients, we collected 200 arterial blood gases (ABG) and simultaneously registered SpO2 levels, as well as hemodynamic and ventilation parameters and vasoactive medication. Patients under therapeutic hypothermia were excluded. Results: The risk of arterial hyperoxia, defined as PaO2 > 100 mm Hg or > 125 mm Hg, was negligible when SpO2 was ≤ 95% or ≤ 96%, respectively. The majority (89% and 54%, respectively for PaO2 > 100 mm Hg and 125 mm Hg) of ICU patients with SpO2 of 100% had arterial hyperoxia. The relation between SpO2 and PaO2 was not clearly affected by hemodynamic or other clinical variables (pH, pCO2, body temperature, recent blood transfusion). Conclusion: In critically ill patients, the prevalence of arterial hyperoxia increases when SpO2 is > 95%. Above this saturation level, supplemental oxygen should be administered with caution in patients potentially susceptible to adverse effects of hyperoxia. HighlightsConcerns have been expressed regarding a possible association between arterial hyperoxia and adverse outcomes in ICU patientsThe risk of hyperoxia, defined as PaO2 > 100mmHg or > 125mmHg, was negligible when SpO2 was ≤ 95% or ≤ 96%, respectivelyThe majority (89% and 54%, respectively for PaO2 > 100mmHg and 125mmHg) of ICU patients with SpO2 of 100% had hyperoxia
Intensive Care Medicine Experimental | 2015
Bob Smit; Yvo M. Smulders; M.C. de Waard; Christa Boer; Aba Vonk; Dennis Veerhoek; Suzanne Kamminga; Hjs de Grooth; Juan J. Garcia-Vallejo; Rjp Musters; Arj Girbes; H.M. Oudemans-van Straaten; Ame Spoelstra-de Man
Hyperoxia is frequently encountered in the intensive care unit (ICU) and during surgical procedures such as coronary artery bypass surgery (CABG). Higher oxygen concentrations intuitively provide a salutary oxygen reserve, but hyperoxia can induce adverse effects such as systemic vasoconstriction, reduction of cardiac output, increased microcirculatory heterogeneity and increased reactive oxygen species production. Previous studies in patients undergoing CABG surgery suggest reduced myocardial damage when avoiding extreme perioperative hyperoxia (>400 mmHg). Here, we compare moderate hyperoxia to near-physiological values.
Clinical Nutrition | 2015
W.G. Looijaard; Sandra N. Stapel; H.M. Oudemans-van Straaten; Peter J.M. Weijs
of their body weight. Logistic regression analysis found that absence of enteral feeding was a risk factor for infectious complications: odds ratio (OR) = 3.8; 95% confidence interval (CI): 1.64 8.79; P= 0.0018; and a risk factor for ICU mortality OR = 2.97; 95%CI 1.02 8.67; P= 0.045. Conclusion: Although the studies and guidelines showed that patients with acute severe pancreatitis should begin EN early, in our clinical practice we still do not use routinely EN in these patients. Failure to use the gastrointestinal (GI) tract in patients with severe acute pancreatitis leads to greater incidence of infectious complications and ICU mortality.
Intensive Care Medicine Experimental | 2014
Bob Smit; M.C. de Waard; Yvo M. Smulders; H.M. Oudemans-van Straaten; Christa Boer; Alexander B.A. Vonk; Dennis Veerhoek; Jj García Vallejo; Suzanne Kamminga; Armand Rj Girbes; A. M. Spoelstra-de Man
Oxidative stress is an important part of a wide range of pathologies and therefore an interesting parameter to determine. However, the detection of reactive oxygen species (ROS), is not straightforward. Sample heterogeneity, delayed analysis and sample preparation, reduces specificity and sensitivity due to probe activation by light, air, probe leakage from cells or cellular activation by sample manipulation. Hence, samples should be processed minimally and analysed immediately if possible. Since clinical research can be subject to uncontrollable timetables and only few departments have access to a dedicated laboratory, the quantification of ROS is challenging.
Clinical Nutrition | 2017
W.G. Looijaard; N. Denneman; B. Broens; Peter J.M. Weijs; H.M. Oudemans-van Straaten
Clinical Nutrition | 2017
M. Guadagni; W.G. Looijaard; M. Tieland; G. Biolo; H.M. Oudemans-van Straaten; Peter J.M. Weijs
Clinical Nutrition | 2017
W.G. Looijaard; N. Denneman; B. Broens; Peter J.M. Weijs; H.M. Oudemans-van Straaten
Clinical Nutrition | 2016
I. Dekker; W.G. Looijaard; H.M. Oudemans-van Straaten; Peter J.M. Weijs