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Research
Early sepsis markers in patients admitted to intensive care unit with moderate to severe diabetic ketoacidosis
Florian Blanchard
Hopital Avicenne
Corresponding Author
ORCiD: https://orcid.org/0000-0001-6545-9566
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Bacterial infections are frequent triggers for diabetic ketoacidosis. In this context, delayed antibiotic treatment is associated with increase morbidity and mortality. Unnecessary administration of antimicrobial therapy might however also negatively impact the prognosis. The usefulness of traditional 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.
Methods
Patients admitted in a single intensive care unit for diabetic ketoacidosis (defined by pH < 7.3 and glycaemia > 13.75mmol/L) were retrospectively analyzed. Clinical and biological markers were evaluated to determine their ability to identify infected from non-infected patients.
Results
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: 3.58ng/mL vs 0.52ng/mL, p<0.001) and presence of fever, defined as temperature > 38°C, (25% vs 2.5%, p=0.007) were different between infected patients and non-infected patients in both univariate and multivariate analysis. Whole blood count, neutrophils count 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 1.44ng/mL leading to a sensibility of 0.90 and a specificity of 0.76. Combining procalcitonin and presence of fever allowed distinguish infected from non-infected patients. Indeed, all patients with procalcitonin level of more than 1.44ng/mL and fever were infected patients. The presence of one of these 2 markers was associated with 46% of infected patients. No afebrile patient with procalcitonin level less than 1.44 ng/mL was infected.
Conclusion
At admission, combining procalcitonin with a threshold above 1.44 ng/mL and presence of fever may be of value to distinguish infected from non-infected patients admitted in intensive care unit for diabetes ketoacidosis.
Keywords
diabetic ketoacidosis, sepsis, bacterial infection, procalcitonin, inflammation, biomarkers
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This is a preprint. It has not completed peer review.
Research
Early sepsis markers in patients admitted to intensive care unit with moderate to severe diabetic ketoacidosis
Florian Blanchard
Hopital Avicenne
Corresponding Author
ORCiD: https://orcid.org/0000-0001-6545-9566
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 18 Dec, 2019
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Critical Care & Emergency Medicine
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Bacterial infections are frequent triggers for diabetic ketoacidosis. In this context, delayed antibiotic treatment is associated with increase morbidity and mortality. Unnecessary administration of antimicrobial therapy might however also negatively impact the prognosis. The usefulness of traditional 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.
Methods
Patients admitted in a single intensive care unit for diabetic ketoacidosis (defined by pH < 7.3 and glycaemia > 13.75mmol/L) were retrospectively analyzed. Clinical and biological markers were evaluated to determine their ability to identify infected from non-infected patients.
Results
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: 3.58ng/mL vs 0.52ng/mL, p<0.001) and presence of fever, defined as temperature > 38°C, (25% vs 2.5%, p=0.007) were different between infected patients and non-infected patients in both univariate and multivariate analysis. Whole blood count, neutrophils count 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 1.44ng/mL leading to a sensibility of 0.90 and a specificity of 0.76. Combining procalcitonin and presence of fever allowed distinguish infected from non-infected patients. Indeed, all patients with procalcitonin level of more than 1.44ng/mL and fever were infected patients. The presence of one of these 2 markers was associated with 46% of infected patients. No afebrile patient with procalcitonin level less than 1.44 ng/mL was infected.
Conclusion
At admission, combining procalcitonin with a threshold above 1.44 ng/mL and presence of fever may be of value to distinguish infected from non-infected patients admitted in intensive care unit for diabetes ketoacidosis.
Figure 1
Figure 2
Figure 3