10 research outputs found

    Diagnostic Errors Induced by a Wrong a Priori Diagnosis: A Prospective Randomized Simulator-Based Trial

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    Preventive strategies against diagnostic errors require the knowledge of underlying mechanisms. We examined the effects of a wrong a priori diagnosis on diagnostic accuracy of a focussed assessment in an acute myocardial infarction scenario. One-hundred-and-fifty-six medical students (cohort 1) were randomized to three study arms differing in the a priori diagnosis revealed: no diagnosis (control group), myocardial infarction (correct diagnosis group), and pulmonary embolism (wrong diagnosis group). Forty-four physicians (cohort 2) were randomized to the control group and the wrong diagnosis group. Primary endpoint was the participants’ final presumptive diagnosis. Among students, the correct diagnosis of an acute myocardial infarction was made by 48/52 (92%) in the control group, 49/52 (94%) in the correct diagnosis group, and 14/52 (27%) in the wrong diagnosis group (p p = 0.023). In the wrong diagnosis group, 31/52 (60%) students and 6/23 (19%) physicians indicated their initially given wrong a priori diagnosis pulmonary embolism as final diagnosis. A wrong a priori diagnosis significantly increases the likelihood of a diagnostic error during a subsequent patient encounter

    Fluid resuscitation does not improve renal oxygenation during hemorrhagic shock in rats

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    Background: The resuscitation strategy for hemorrhagic shock remains controversial, with the kidney being especially prone to hypoxia. Methods: The authors used a three-phase hemorrhagic shock model to investigate the effects of fluid resuscitation on renal oxygenation. After a 1-h shock phase, rats were randomized into four groups to receive either normal saline or hypertonic saline targeting a mean arterial pressure (MAP) of either 40 or 80 mmHg. After such resuscitation, rats were transfused with the shed blood. Renal macro-and microcirculation were monitored with cortical and outer-medullary microvascular oxygen pressure, renal oxygen delivery, and renal oxygen consumption measured using oxygen-dependent quenching of phosphorescence. Results: Hemorrhagic shock was characterized by a drop of aortic blood flow, MAP, renal blood flow, renal oxygen delivery, renal oxygen consumption, and renal microvascular PO2. During the fluid resuscitation phase, normal saline targeting a MAP = 80 mmHg was the sole strategy able to restore aortic blood flow, renal blood flow, and renal oxygen consumption, although without improving renal oxygen delivery. However, none of the strategies using either normal saline or hypertonic saline or targeting a high MAP could restore the renal microvascular Po2. Blood transfusion increased microvascular Po2 but was unable to totally restore renal microvascular oxygenation to baseline values. Conclusions: This experimental rat study shows that (1) high MAP-directed fluid resuscitation (80 mmHg) does not lead to higher renal microvascular Po2 compared with fluid resuscitation targeted to MAP (40 mmHg); (2) hypertonic saline is not superior to normal saline regarding renal oxygenation; and (3) decreased renal oxygenation persists after blood transfusion

    Mitochondrial oxygen tension within the heart

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    By using a newly developed optical technique which enables non-invasive measurement of mitochondrial oxygenation (mitoPO2) in the intact heart, we addressed three long-standing oxygenation questions in cardiac physiology: 1) what is mitoPO2 within the in vivo heart?, 2) is mitoPO2 heterogeneously distributed?, and 3) how does mitoPO2 of the isolated Langendorff-perfused heart compare with that in the in vivo working heart? Following calibration and validation studies of the optical technique in isolated cardiomyocytes, mitochondria and intact hearts, we show that in the in vivo condition mean mitoPO2 was 35 ± 5 mm Hg. The mitoPO2 was highly heterogeneous, with the largest fraction (26%) of mitochondria having a mitoPO2 between 10 and 20 mm Hg, and 10% between 0 and 10 mm Hg. Hypoxic ventilation (10% oxygen) increased the fraction of mitochondria in the 0–10 mm Hg range to 45%, whereas hyperoxic ventilation (100% oxygen) had no major effect on mitoPO2. For Langendorff-perfused rat hearts, mean mitoPO2 was 29 ± 5 mm Hg with the largest fraction of mitochondria (30%) having a mitoPO2 between 0 and 10 mm Hg. Only in the maximally vasodilated condition, did the isolated heart compare with the in vivo heart (11% of mitochondria between 0 and 10 mm Hg). These data indicate 1) that the mean oxygen tension at the level of the mitochondria within the heart in vivo is higher than generally considered, 2) that mitoPO2 is considerably heterogeneous, and 3) that mitoPO2 of the classic buffer-perfused Langendorff heart is shifted to lower values as compared to the in vivo heart

    Thyroid hemorrhage causing airway obstruction after intravenous thrombolysis for acute ischemic stroke

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    There are several life-threatening complications associated with intravenous thrombolysis after acute ischemic stroke such as symptomatic intracerebral hemorrhage, orolingual angioedema, or less frequent, bleedings of the mucosa or ecchymosis. Aside from these known critical incidents, rare and unfamiliar complications may be even more challenging, as they are unexpected and may mimic events that appear more frequently. We report a rare and unusual acute complication of intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA) (0.9 mg/kg) administered for acute ischemic stroke.; Medical records, radiologic imaging, and pathologic specimens were reviewed.; A 86-year-old woman developed acute respiratory failure 20 h after thrombolysis with suspected angioedema triggered by intravenous rt-PA. The inspiratory stridor and dyspnea were unresponsive to bronchodilators, corticosteroids, and inhaled adrenaline. After endotracheal intubation, laryngoscopy showed no significant supraglottic narrowing. Thyroidal sonography and cervical computed tomography revealed a thyroidal mass causing a tracheal and vascular compression compatible with thyroidal hemorrhage. Sonography showed a nodular goiter of the right thyroid gland. A total thyroidectomy was performed and histologic analysis confirmed a hemorrhage of the right thyroidal lobe.; Acute airway obstruction with respiratory failure due to thyroidal hemorrhage after intravenous thrombolysis is an important life-threatening complication, mimicking an anaphylactic reaction or a more frequent orolingual angioedema

    International study on microcirculatory shock occurrence in acutely Ill patients

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    Objectives: Microcirculatory alterations are associated with adverse outcome in subsets of critically ill patients. The prevalence and significance of microcirculatory alterations in the general ICU population are unknown. We studied the prevalence of microcirculatory alterations in a heterogeneous ICU population and its predictive value in an integrative model of macro- and microcirculatory variables. Design: Multicenter observational point prevalence study. Setting: The Microcirculatory Shock Occurrence in Acutely ill Patients study was conducted in 36 ICUs worldwide. Patients: A heterogeneous ICU population consisting of 501 patients. Interventions: None. Measurements and Main Results: Demographic, hemodynamic, and laboratory data were collected in all ICU patients who were 18 years old or older. Sublingual Sidestream Dark Field imaging was performed to determine the prevalence of an abnormal capillary microvascular flow index ( 90 beats/min) (odds ratio, 2.71; 95% CI, 1.67-4.39; p < 0.001), mean arterial pressure (odds ratio, 0.979; 95% CI, 0.963-0.996; p = 0.013), vasopressor use (odds ratio, 1.84; 95% CI, 1.11-3.07; p = 0.019), and lactate level more than 1.5 mEq/L (odds ratio, 2.15; 95% CI, 1.28-3.62; p = 0.004) were independent risk factors for hospital mortality, but not abnormal microvascular flow index. In reference to microvascular flow index, a significant interaction was observed with tachycardia. In patients with tachycardia, the presence of an abnormal microvascular flow index was an independent, additive predictor for in-hospital mortality (odds ratio, 3.24; 95% CI, 1.30-8.06; p = 0.011). This was not true for nontachycardic patients nor for the total group of patients. Conclusions: In a heterogeneous ICU population, an abnormal microvascular flow index was present in 17% of patients. This was not associated with mortality. However, in patients with tachycardia, an abnormal microvascular flow index was independently associated with an increased risk of hospital death

    Private Equity funds and their performance in the post-crisis period

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    The work covers the topic of private equity funds performance and attempt to identify the impact of macroeconomic conditions on the entire industry. The recent central banks' actions put a question about the impact of changes in interest rates on the private equity funds performance. With the sample of 100 observations provided by Cambridge Associates, we identified the significant negative effect of prevailing low interest rates on the growth of private equity funds performance. We further attempt to answer the question, whether private equity funds operating in post-crisis years has on average higher growth rate, however, we could not provide the answer as we failed to reject the null, neutral effect hypothesis. Additionally, with a sample of 3092 observations provided by Bloomberg, we found that the effect of cheap debt has increased on average in the postcrisis period, predicting that the private equity performance can suffer once the interest rates rises enough

    International Study on Microcirculatory Shock Occurrence in Acutely Ill Patients

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    International Study on Microcirculatory Shock Occurrence in Acutely Ill Patients

    No full text
    Objectives: Microcirculatory alterations are associated with adverse outcome in subsets of critically ill patients. the prevalence and significance of microcirculatory alterations in the general ICU population are unknown. We studied the prevalence of microcirculatory alterations in a heterogeneous ICU population and its predictive value in an integrative model of macro- and microcirculatory variables.Design: Multicenter observational point prevalence study.Setting: the Microcirculatory Shock Occurrence in Acutely ill Patients study was conducted in 36 ICUs worldwide.Patients: A heterogeneous ICU population consisting of 501 patients.Interventions: None.Measurements and Main Results: Demographic, hemodynamic, and laboratory data were collected in all ICU patients who were 18 years old or older. Sublingual Sidestream Dark Field imaging was performed to determine the prevalence of an abnormal capillary microvascular flow index ( 90 beats/min) (odds ratio, 2.71; 95% CI, 1.67-4.39; p < 0.001), mean arterial pressure (odds ratio, 0.979; 95% CI, 0.963-0.996; p = 0.013), vasopressor use (odds ratio, 1.84; 95% CI, 1.11-3.07; p = 0.019), and lactate level more than 1.5 mEq/L (odds ratio, 2.15; 95% CI, 1.28-3.62; p = 0.004) were independent risk factors for hospital mortality, but not abnormal microvascular flow index. in reference to microvascular flow index, a significant interaction was observed with tachycardia. in patients with tachycardia, the presence of an abnormal microvascular flow index was an independent, additive predictor for in-hospital mortality (odds ratio, 3.24; 95% CI, 1.30-8.06; p = 0.011). This was not true for nontachycardic patients nor for the total group of patients.Conclusions: in a heterogeneous ICU population, an abnormal microvascular flow index was present in 17% of patients. This was not associated with mortality. However, in patients with tachycardia, an abnormal microvascular flow index was independently associated with an increased risk of hospital death.Erasmus MC Univ Med Ctr, Dept Intens Care Adults, Rotterdam, NetherlandsMed Ctr Leeuwarden, Dept Intens Care, Leeuwarden, NetherlandsUniv Politecn Marche, Dept Biomed Sci & Publ Hlth, Ancona, ItalyServ Terapia Intens Sanatorio Otamendi & Miroli, Buenos Aires, DF, ArgentinaBeth Israel Deaconess Med Ctr, Dept Emergency Med, Boston, MA 02215 USABeth Israel Deaconess Med Ctr, Vasc Biol Res Ctr, Boston, MA 02215 USABarts & London Queen Marys Sch Med & Dent, London, EnglandUniversidade Federal de São Paulo, São Paulo, BrazilUniv Klinikum RWTH Aachen, Klin Anesthesiol, Aachen, GermanyKosuyolu Univ, K Kosuyolu High Specialty Educ & Res Hosp, Istanbul, TurkeyLithuanian Univ Hlth Sci, Dept Intens Care, Kaunas, LithuaniaCooper Univ Hosp, Sect Cardiol, Camden, NJ USAUniv Basel Hosp, Med Intens Care Unit, CH-4031 Basel, SwitzerlandSt Antonius Hosp, Dept Anesthesiol Intens Care & Pain Manag, Nieuwegein, NetherlandsOnze Lieve Vrouw Hosp, Dept Intens Care, Amsterdam, NetherlandsSt Louis Univ Hosp, Mercy Hosp St Louis, St Louis, MO USAUniv Plymouth, Peninsula Sch Med, Derriford Hosp, Plymouth PL4 8AA, Devon, EnglandHacettepe Univ, Intens Care Unit, Ankara, TurkeyUDELAR, Sch Med, Hosp Espanol ASSE, Intens Care Unit, Montevideo, UruguayNew Cross Hosp, Intens Care Unit, Wolverhampton, W Midlands, EnglandUniv Paris 07, Hop Lariboisiere, AP HP, Dept Anesthesiol Crit Care & SMUR, Paris, FranceCanberra Hosp, Intens Care Unit, Canberra, ACT, AustraliaRoyal Brisbane & Womens Hosp, Dept Intens Care Med, Brisbane, Qld, AustraliaIspat Hosp, Intens Care Unit, Rourkela, Orissa, IndiaUniv Pittsburgh, Pittsburgh, PA USAUniv Calif San Diego, Sch Med, San Diego, CA 92103 USAJoan XXIII Univ Hosp, Dept Crit Care, Tarragona, SpainPontificia Univ Catolica Chile, Fac Med, Escuela Med, Dept Med Intens, Santiago, ChileHosp San Martin, Intens Care Unit, La Plata, Buenos Aires, ArgentinaUniv Paris 11, Hop Bicetre, AP HP, Hop Univ Paris Sud,Dept Anesthesie Reanimat, Paris, FranceGelre Ziekenhuizen, Intens Care Unit, Apeldoorn, NetherlandsRoyal Marsden Hosp, Intens Care Unit, London SW3 6JJ, EnglandRoyal Devon & Exeter Hosp, Intens Care Unit, Exeter EX2 5DW, Devon, EnglandSanta Maria Angeli Hosp, Intens Care Unit, Pordenone, ItalyUniv Jena, Univ Klinikum Jena, Dept Internal Med 1, Jena, GermanyRoyal Free Hosp, Intens Care Unit, London NW3 2QG, EnglandDipartimento Anestesia Rianimaz & Terapia Intens, Treviso, ItalyUniv Amsterdam, Acad Med Ctr, Dept Cardiol, NL-1105 AZ Amsterdam, NetherlandsUniversidade Federal de São Paulo, São Paulo, BrazilWeb of Scienc
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