Accuracy of Laboratory Data Communication on ICU Daily Rounds Using an Electronic Health Record.

OBJECTIVES: Accurately communicating patient data during daily ICU rounds is critically important since data provide the basis for clinical decision making. Despite its importance, high fidelity data communication during interprofessional ICU rounds is assumed, yet unproven. We created a robust but simple methodology to measure the prevalence of inaccurately communicated (misrepresented) data and to characterize data communication failures by type. We also assessed how commonly the rounding team detected data misrepresentation and whether data communication was impacted by environmental, human, and workflow factors. DESIGN: Direct observation of verbalized laboratory data during daily ICU rounds compared with data within the electronic health record and on presenters' paper prerounding notes. SETTING: Twenty-six-bed academic medical ICU with a well-established electronic health record. SUBJECTS: ICU rounds presenter (medical student or resident physician), interprofessional rounding team. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: During 301 observed patient presentations including 4,945 audited laboratory results, presenters used a paper prerounding tool for 94.3% of presentations but tools contained only 78% of available electronic health record laboratory data. Ninty-six percent of patient presentations included at least one laboratory misrepresentation (mean, 6.3 per patient) and 38.9% of all audited laboratory data were inaccurately communicated. Most misrepresentation events were omissions. Only 7.8% of all laboratory misrepresentations were detected. CONCLUSION: Despite a structured interprofessional rounding script and a well-established electronic health record, clinician laboratory data retrieval and communication during ICU rounds at our institution was poor, prone to omissions and inaccuracies, yet largely unrecognized by the rounding team. This highlights an important patient safety issue that is likely widely prevalent, yet underrecognized.

Treatment of anemia in patients with heart disease: a systematic review.

BACKGROUND: The benefits of anemia treatment in patients with heart disease are uncertain. PURPOSE: To evaluate the benefits and harms of treatments for anemia in adults with heart disease. DATA SOURCES: MEDLINE, EMBASE, and Cochrane databases; clinical trial registries; reference lists; and technical advisors. STUDY SELECTION: English-language trials of blood transfusions, iron, or erythropoiesis-stimulating agents in adults with anemia and congestive heart failure or coronary heart disease and observational studies of transfusion. DATA EXTRACTION: Data on study design, population characteristics, hemoglobin levels, and health outcomes were extracted. Trials were assessed for quality. DATA SYNTHESIS: Low-strength evidence from 6 trials and 26 observational studies suggests that liberal transfusion protocols do not improve short-term mortality rates compared with less aggressive protocols (combined relative risk among trials, 0.94 [95% CI, 0.61 to 1.42]; I2 = 16.8%), although decreased mortality rates occurred in a small trial of patients with the acute coronary syndrome (1.8% vs. 13.0%; P = 0.032). Moderate-strength evidence from 3 trials of intravenous iron found improved short-term exercise tolerance and quality of life in patients with heart failure. Moderate- to high-strength evidence from 17 trials of erythropoiesis-stimulating agent therapy found they offered no consistent benefits, but their use may be associated with harms, such as venous thromboembolism. LIMITATIONS: Few trials have examined transfusions in patients with heart disease, and observational studies are potentially confounded by indication. Data supporting iron use come mainly from 1 large trial, and long-term effects are unknown. CONCLUSION: Higher transfusion thresholds do not consistently improve mortality rates, but large trials are needed. Intravenous iron may help to alleviate symptoms in patients with heart failure and iron deficiency and also warrants further study. Erythropoiesis-stimulating agents do not seem to benefit patients with mild to moderate anemia and heart disease and may be associated with serious harms. PRIMARY FUNDING SOURCE: U.S. Department of Veterans Affairs.

Early brain swelling in acute hypoxia.

Acute mountain sickness (AMS) and high-altitude cerebral edema share common clinical characteristics, suggesting cerebral swelling may be an important factor in the pathophysiology of AMS. Hypoxia and hypocapnia associated with high altitude are known to exert strong effects on the control of the cerebral circulation, yet how these effects interact during acute hypoxia, and whether AMS-susceptible subjects may have a unique response, is still unclear. To test if self-identified AMS-susceptible individuals show altered brain swelling in response to acute hypoxia, we used quantitative arterial spin-labeling and volumetric MRI to measure cerebral blood flow and cerebrospinal fluid (CSF) volume changes during 40 min of acute hypoxia. We estimated changes in cerebral blood volume (CBV) (from changes in cerebral blood flow) and brain parenchyma swelling (from changes in CBV and CSF). Subjects with extensive high-altitude experience in two groups participated: self-identified AMS-susceptible (n = 6), who invariably experienced AMS at altitude, and self-identified AMS-resistant (n = 6), who almost never experienced symptoms. During 40-min hypoxia, intracranial CSF volume decreased significantly [-10.5 ml (SD 6.9), P < 0.001]. There were significant increases in CBV [+2.3 ml (SD 2.5), P < 0.005] and brain parenchyma volume [+8.2 ml (SD 6.4), P < 0.001]. However, there was no significant difference between self-identified AMS-susceptible and AMS-resistant groups for these acute-phase changes. In acute hypoxia, brain swelling occurs earlier than previously described, with significant shifts in intracranial CSF occurring as early as 40 min after exposure. These acute-phase changes are present in all individuals, irrespective of susceptibility to AMS.

Regional cerebral blood flow during acute hypoxia in individuals susceptible to acute mountain sickness.

UNLABELLED: Individuals susceptible to high altitude pulmonary edema show altered pulmonary vascular responses within minutes of exposure to hypoxia. We hypothesized that a similar acute-phase vulnerability to hypoxia may exist in the brain of individuals susceptible to acute mountain sickness (AMS). In established AMS and high altitude cerebral edema, there is a propensity for vasogenic white matter edema. We therefore hypothesized that increased cerebral blood flow (CBF) during acute hypoxia would also be disproportionately greater in white matter (WM) than grey matter (GM) in AMS-susceptible subjects. We quantified regional CBF using arterial spin labeling MRI during 30 min hypoxia (F(I)O(2) = 0.125) in two groups: AMS-susceptible (AMS-S, n = 6) who invariably experienced AMS at altitude, and AMS-resistant (AMS-R, n = 6) who never experienced AMS despite multiple rapid ascents to high altitude. SaO(2) during hypoxia did not differ between groups (AMS-S = 87+/-4%, AMS-R = 89+/-3%, p = 0.3). Steady-state whole-brain CBF increased in hypoxia (p<0.005), but did not differ between groups (normoxia: AMS-S = 42.7+/-14.0 ml/(100 g min), AMS-R = 41.7+/-10.1 ml/(100 g min); hypoxia: AMS-S = 47.8+/-19.5 ml/(100 g min), AMS-R = 48.2+/-10.1 ml/(100 g min), p = 0.65), and cerebral oxygen delivery remained constant. The percent change in CBF did not differ between brain regions or between groups (although absolute CBF change was greater in GM): (GM: AMS-S = 6.1+/-7.7 ml/(100 g min) (10+/-11%), AMS-R = 8.3+/-5.7 ml/(100 g min) (17+/-11%), p = 0.57; WM: AMS-S = 4.3+/-5.1 ml/(100 g min) (12+/-15%), AMS-R = 4.8+/-2.9 ml/(100 g min) (16+/-9%), p = 0.82). CONCLUSION: CBF increases in acute hypoxia, but is not different between WM and GM, irrespective of AMS susceptibility. Acute phase differences in regional CBF during acute hypoxia are not a primary feature of susceptibility to AMS.