Dorian Leroy, Bruno Sirault, Alexandre Rousseau, Patrick Biston, Karim Zouaoui Boudjeltia, Michaël Piagnerelli
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引用次数: 0
Abstract
Background: Diabetic ketoacidosis (DKA) is a life-threatening emergency. Microvascular hyporeactivity has been reported in these patients and is completely reversible when acidosis is corrected with aggressive treatment. The shape of the red blood cell (RBC), a sensor of local hypoxia and a component of the microcirculation, is altered in diabetic patients, but no data are available concerning RBC deformability in DKA during treatment.
Methods: In this prospective observational study, we included all adult patients admitted with DKA to a 32-bed medico-surgical ICU over a 6-month period. We excluded patients with infection. We measured RBC deformability in the DKA patients and compared results with those from patients with type 1 diabetes (DM1) and from a group of healthy volunteers (HV). RBC deformability was assessed using ektacytometry. In the DKA patients, it was assessed at ICU admission, 8 and 24 hours after admission, and prior to ICU discharge (48-72 h). The RBC elongation index (EI) was determined based on the laser diffraction pattern changes. A higher EI indicates greater RBC deformability.
Results: A total of 46 diabetic patients (15 DKA and 31 DM1 patients) and 20 HV were included. RBC deformability was more altered at ICU admission in DKA patients, with significantly lower EI values than in the other groups, and these alterations persisted during the ICU stay despite treatment. There were no correlations between these alterations and the quantity of fluids or insulin received.
Conclusions: In contrast to the reversible microvascular hyporeactivity observed in DKA, RBC deformability was already altered at ICU admission in patients with DKA and remained altered despite treatment. These alterations may contribute to the blood flow abnormalities observed in these patients.
期刊介绍:
SHOCK®: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches includes studies of novel therapeutic approaches, such as immunomodulation, gene therapy, nutrition, and others. The mission of the Journal is to foster and promote multidisciplinary studies, both experimental and clinical in nature, that critically examine the etiology, mechanisms and novel therapeutics of shock-related pathophysiological conditions. Its purpose is to excel as a vehicle for timely publication in the areas of basic and clinical studies of shock, trauma, sepsis, inflammation, ischemia, and related pathobiological states, with particular emphasis on the biologic mechanisms that determine the response to such injury. Making such information available will ultimately facilitate improved care of the traumatized or septic individual.