RESUMO
OBJECTIVES: The current standard of care to deliver invasive mechanical ventilation support is the protective ventilation approach. One pillar of this approach is the limitation of tidal volume to less than 6 mL/Kg of predicted body weight. Predicted body weight is calculated from patient's height. Yet, little is known about the potential impact of errors arising from visual height estimation, a common practice, to calculate tidal volumes. The aim of this study was to evaluate that impact on tidal volume calculation to use during protective ventilation. DESIGN: Prospective observational study. SETTING: An eight-bed polyvalent ICU. PATIENTS: Adult patients (≥ 18 yr). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Tidal volumes were calculated from visual height estimates made by physicians, nurses, and patients themselves and compared with tidal volumes calculated from measured heights. Comparisons were made using the paired t test. Modified Bland-Altman plots were used to assess agreement between height estimates and measurements. One-hundred patients were recruited. Regardless of the height estimator, all the mean tidal volumes would be greater than 6 mL/Kg predicted body weight (all p < 0.001). Additionally, tidal volumes would be greater than or equal to 6.5 mL/Kg predicted body weight in 18% of patients' estimates, 25% of physicians' estimates, and 30% of nurses' estimates. Patients with lower stature (< 165 cm), older age, and surgical typology of admission were at increased risk of being ventilated with tidal volumes above protective threshold. CONCLUSIONS: The clinical benefit of the protective ventilation strategy can be offset by using visual height estimates to calculate tidal volumes. Additionally, this approach can be harmful and potentially increase mortality by exposing patients to tidal volumes greater than or equal to 6.5 mL/Kg predicted body weight. In the interest of patient safety, every ICU patient should have his or her height accurately measured.
RESUMO
Lupus nephritis (LN) affects up to 50% of patients with Systemic Lupus Erythematosus (SLE) and is associated with a worse prognosis. LN usually develops within the first 5 years of the onset of the disease. We report three patients with very delayed LN (DLN) diagnosed after 15 or more years after SLE diagnosis. The three patients were non-Caucasian women with adolescent or adult-onset SLE. Each had antinuclear, anti-dsDNA and anti-Ro antibodies. Hydroxychloroquine was prescribed for each. Their disease courses were characterised by sporadic non-renal flares controlled by steroids and, in two cases, by one cycle of rituximab. Unexpectedly, they developed proteinuria, haematuria and lowering of estimated glomerular filtration rate with clinical signs of renal disease. LN was confirmed by renal biopsy. Reviewing them, each showed serological signs of increasing disease activity (rising levels of anti-dsDNA antibodies and fall in C3) that predated clinical or laboratory signs of LN by 1-3 years. Reviewing the literature, we found a lack of knowledge about DLN starting more than 15 years after SLE diagnosis. With the increasing life expectancy of patients with SLE it is likely that more cases of very DLN will emerge.
