Blanchard Florian, Charbit Judith, Van der Meersch Guillaume, Popoff Benjamin, Picod Adrien, Cohen Regis, Chemouni Frank, Gaudry Stephane, Bihan Helene, Cohen Yves
Medical-Surgical Intensive Care Unit, Avicenne University Hospital, AP-HP, Paris 13 University, Sorbonne Paris Cité, 125 rue Stalingrad, 93000, Bobigny, France.
Department of Endocrinology, Diabetology, Metabolic Disease, Avicenne University Hospital, AP-HP, Paris 13 University, Sorbonne Paris Cité, CRNH-IdF, 125 rue Stalingrad, Bobigny, France.
Ann Intensive Care. 2020 May 19;10(1):58. doi: 10.1186/s13613-020-00676-6.
Bacterial infections are frequent triggers for diabetic ketoacidosis. In this context, delayed antibiotic treatment is associated with increased morbidity and mortality. Unnecessary administration of antimicrobial therapy might however, also negatively impact the prognosis. The usefulness of sepsis markers in diabetic ketoacidosis has not been assessed. Thus, we sought to investigate diagnostic performances of clinical and biological sepsis markers during diabetic ketoacidosis.
In this monocentric retrospective cohort study, all consecutive episodes of diabetic ketoacidosis (defined as pH ≤ 7.25, glycaemia > 300 mg/dL and presence of ketones) admitted in intensive care unit were included. A proven bacterial infection was defined as bacteriological documentation on any bacterial sample. Clinical (presence of fever: temperature > 38 °C and presence of hypothermia: temperature < 36 °C) and biological markers (whole blood count, neutrophils count, neutrophils-to-lymphocytes count ratio and procalcitonin), recorded at admission, were compared according to the presence or absence of a proven bacterial infection.
Between 2011 and 2018, among 134 episodes of diabetic ketoacidosis, 102 were included (91 patients). Twenty out of 102 were infected. At admission, procalcitonin (median: 3.58 ng/mL vs 0.52 ng/mL, p < 0.001) and presence of fever (25% vs 44%, p = 0.007) were different between episodes with and without proven bacterial infection in both univariate and multivariate analysis. Whole blood count, neutrophils count, neutrophils-to-lymphocytes count ratio and presence of hypothermia were not different between both groups. The diagnostic performance analysis for procalcitonin revealed an area under the curve of 0.87 with an optimal cutoff of 1.44 ng/mL leading to a sensitivity of 0.90 and a specificity of 0.76. Combining procalcitonin and presence of fever allowed to distinguish proven bacterial infection episodes from those without proven bacterial infection. Indeed, all patients with procalcitonin level of more than 1.44 ng/mL and fever had proven bacterial infection episodes. The presence of one of these 2 markers was associated with 46% of proven bacterial infection episodes. No afebrile patient with procalcitonin level less than 1.44 ng/mL had a proven bacterial infection.
At admission, combining procalcitonin and presence of fever may be of value to distinguish ketoacidosis patients with and without proven bacterial infection, admitted in intensive care unit.
细菌感染是糖尿病酮症酸中毒常见的诱因。在此情况下,抗生素治疗延迟与发病率和死亡率增加相关。然而,不必要的抗菌治疗也可能对预后产生负面影响。目前尚未评估脓毒症标志物在糖尿病酮症酸中毒中的作用。因此,我们旨在研究糖尿病酮症酸中毒期间临床和生物学脓毒症标志物的诊断效能。
在这项单中心回顾性队列研究中,纳入了重症监护病房收治的所有连续性糖尿病酮症酸中毒发作病例(定义为pH≤7.25、血糖>300mg/dL且存在酮体)。确诊的细菌感染定义为任何细菌样本的细菌学记录。比较入院时记录的临床指标(发热:体温>38°C和体温过低:体温<36°C)和生物学标志物(全血细胞计数、中性粒细胞计数、中性粒细胞与淋巴细胞计数比值和降钙素原)在有无确诊细菌感染情况下的差异。
2011年至2018年期间,在134例糖尿病酮症酸中毒发作病例中,纳入了102例(91名患者)。102例中有20例发生感染。入院时,单因素和多因素分析显示,有确诊细菌感染和无确诊细菌感染的发作病例之间,降钙素原(中位数:3.58ng/mL对0.52ng/mL,p<0.001)和发热情况(25%对44%,p=0.007)存在差异。两组之间全血细胞计数、中性粒细胞计数、中性粒细胞与淋巴细胞计数比值和体温过低情况无差异。降钙素原的诊断效能分析显示曲线下面积为0.87,最佳截断值为1.44ng/mL,敏感性为0.90,特异性为0.76。联合降钙素原和发热情况能够区分确诊细菌感染发作病例和无确诊细菌感染发作病例。事实上,所有降钙素原水平超过1.44ng/mL且发热的患者均有确诊细菌感染发作病例。这两种标志物中出现一种与46%的确诊细菌感染发作病例相关。降钙素原水平低于1.44ng/mL且无发热的患者均无确诊细菌感染。
入院时,联合降钙素原和发热情况对于区分重症监护病房收治的有无确诊细菌感染的酮症酸中毒患者可能具有价值。