Procalcitonin PCT is actually one of the major relevant markers for the diagnosis of bacterial infections. PCT is daily used for antibiotic decisions in patients with respiratory tract infections and sepsis [ 13 , 14 , 15 ].
Nevertheless, some preliminary data suggest that compared with non-diabetics, PCT positive threshold could be higher in diabetic patients, especially during hyperglycemic crisis [ 16 , 17 ]. We therefore conducted a retrospective study in which we sought to investigate the diagnostic performance of different sepsis markers including PCT to predict bacterial infection in the first 2 days of admission in intensive care unit ICU for DKA.
This was a retrospective study performed in the ICU of Avicenne hospital, a French tertiary hospital, in the Paris area. All consecutive patients hospitalized for moderate-to-severe DKA between January and March were included.
Patients were not included if they had one or more criteria known to increase PCT without any indication of bacterial infection medullary thyroid carcinoma, small cell lung cancer, cardiac arrest, heat stroke, pancreatitis, malaria, notion of fungal infection, severe trauma [ 19 ].
As a retrospective study of routinely collected and anonymized data, consent was not required, and patients were only informed by letter of their enrollment in the studies.
From charts, we extracted the following data at admission D0 : clinical parameters such as history and type of diabetes, comorbidities, diabetes complications, medication, temperature, and biological data such as pH, bicarbonate, first glycemia available either by venous or capillary blood punctures , ketonemia, sepsis markers see below.
A follow-up of those parameters was collected on day 2 D2 when available. Clinical and biological sepsis markers were assessed on D0 and D2. As part of the systemic inflammatory response syndrome, temperature and white blood cell count were collected. From the whole blood count, white blood cell count WBC , neutrophil blood count and neutrophils-to-lymphocytes count ratio NLCR were extracted. PCT concentration was considered normal if below 0. C-reactive protein was not collected due to the high number of missing data.
Bacterial samples were only requested in case of suspected infection. We performed a univariate analysis to compare these 2 subgroups of patients. We performed a multivariate logistic regression analysis to assess the relationship between sepsis markers and infection status. As sepsis markers on D0 and D2 are coupled, we used 2 different models integrating the significant variables at each time point D0 and D2.
The multivariate analysis was done on a complete case analysis. A sensitivity analysis with a multiple imputation was achieved to deal with missing data. Receiver operating characteristics ROC curves analysis was performed to assess the ability of sepsis markers to predict infection.
Optimal cutoff values were chosen to maximize sensitivity and specificity using the Youden index. Statistical analyses were carried out using R version 3. We did not include 32 episodes 29 patients because of the absence of eligibility criteria, wrong coding diagnosis or missing data Fig. The remaining episodes 91 patients were included in the analysis. At ICU admission, median pH and bicarbonate were 7. On D2, ketoacidosis was corrected as shown by a median pH of 7. On D2, correction of DKA was similar in both groups.
Those 16 episodes were included in the study on the basis of the presence of ketones in urine. A sensitivity analysis with multiple imputation for missing ketonemia data confirmed the previous multivariate analysis.
The optimal threshold was obtained at 1. The AUC for temperature was 0. Receiver operating characteristics curve of procalcitonin PCT a and temperature b at admission. Positive and negative likelihood ratios were 3. For temperature, the area under curve AUC was 0.
Positive and negative likelihood ratios were 1. All episodes with a PCT level of more than 1. No afebrile patient with PCT level less than 1. Procalcitonin PCT and fever as markers of proven bacterial infection at admission.
On D2, more differences appeared between the two groups. This is the first study to assess the diagnostic performance of different sepsis markers to predict proven bacterial infection for patients with DKA, admitted in ICU.
Fever and high PCT threshold above 1. The only clinical marker was temperature. Nevertheless, in episodes without PBI, body temperature ranged from This huge variation may be explained by thermoregulatory function impairment in diabetic patients [ 22 ]. In Gale et al. Hypothermia was also associated with infection [ 24 ].
In our study, we neither found an increase in mortality nor an association with sepsis for hypothermic patients. Other classical sepsis markers were also found to be inefficient in our study to differentiate PBI episodes from those without PBI.
Such leukocytosis, as high as This result leads to reconsider the usefulness of WBC to predict bacterial infection at admission. Recently, the NLCR was proposed to be a more useful diagnostic tool than other blood tests to identify patients with bacterial infection [ 27 ].
However, in our study we did not highlight any difference for this marker between both groups at admission. PCT, a precursor of calcitonin, is generated as part of the systemic response to bacterial infections [ 28 ]. Our study emphasized the relevance of PCT to predict infection, with a good predictive value above the level of 1. In febrile patients admitted in the emergency department, Hausfater et al. Wacker et al. Sager et al. However, the positive threshold seems to be higher than usual in our study optimal cutoff on D0: 1.
Previous studies already reported huge cutoff heterogeneity. For example, Wacker et al. However, a participation of the hyperglycemic crisis in the increase of the PCT could not be excluded. Indeed, Aksu et al. In our study, we found an elevated a high level of PCT in patients without any proven bacterial infection, with a PCT drop following normalization of glycemia.
High PCT levels were recently reported in different case reports or case series focusing on diabetes ketoacidosis without infection [ 33 , 34 ].
This is why immunizations for influenza the flu and pneumococcal disease are recommended for people who have diabetes. And people who have high blood sugar from diabetes are more likely to be infected with unusual organisms, such as Gram-negative bacteria or fungi. Foot infections are common in people who have high blood sugar from diabetes. Nerve damage neuropathy combined with poor blood supply to the feet puts people who have high blood sugar from diabetes at high risk for infected foot ulcers.
Other infections for which people with high blood sugar from diabetes are at increased risk include:. Author: Healthwise Staff. Medical Review: E. This information does not replace the advice of a doctor. DKA should be treated as a medical emergency. This is because it can lead to coma or death. If you have the symptoms of DKA, get medical help right away.
DKA happens more often in people with type 1 diabetes. But it can happen in people with type 2 diabetes. It can also happen in women with diabetes during pregnancy. This is often known as gestational diabetes. DKA happens when insulin levels are too low. The glucose stays in the blood. This causes high blood glucose hyperglycemia. Without glucose, your body breaks down stored fat for energy.
When this happens, acids called ketones are released into the blood. This is known as ketosis. Revision received:. Select Format Select format. Permissions Icon Permissions. Abstract We determined the prevalence and indicators of infection in intensive care unit ICU patients with diabetic ketoacidosis DKA by performing a retrospective analysis of episodes of DKA in patients managed in a medical ICU between and Open in new tab Download slide. Google Scholar Crossref.
Search ADS. Therapy of severe diabetic ketoacidosis: zero mortality under very low-dose insulin application. Google Scholar PubMed. Diabetes in urban African-Americans: cessation of insulin therapy is the major precipitating cause of diabetic ketoacidosis. Neutrophil bactericidal function in diabetes mellitus: evidence for association with blood glucose control.
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