Fresh frozen plasma is permissive for systemic inflammatory response syndrome, infection, and sepsis in multiple-injured patients.

BACKGROUND: The correction of coagulopathy with fresh frozen plasma (FFP) is one of the main issues in the treatment of multiple-injured patients. Infectious and septic complications contribute to an adverse outcome in multiple-injured patients. Here, we investigated the role of FFP in the development of inflammatory complications given within the first 48 hours. METHODS: A total of 2033 patients with multiple injuries and an Injury Severity Score greater than 16 points and aged 16 years or older were included. The population was subdivided into 2 groups: those who received FFP and those who did not. The data were analyzed using SPSS version 22.0. Associations between the data were tested using Pearson correlation. Independent predictivity was analyzed by binary logistic regression and multivariate regression. Data were considered as significant if P<.05. RESULTS: The prothrombin time at admission was significantly lower (68.5%±23.3% vs 81.8%±21.0% normal; P<.001) in the group receiving FFP. The application of FFP led to a more severe systemic inflammatory response syndrome (SIRS) grade (3.0±1.2 vs 2.2±1.4; P<.001), to a higher infection rate (48% vs 28%; P<.001), and to a higher sepsis rate (29% vs 13%; P<.001) in the patients receiving FFP. The correlations between SIRS and the incidence of infections and sepsis increased with the amount of FFP applied (P<.001). CONCLUSIONS: Treatment with FFP of bleeding patients with multiple injuries enhances the risk of SIRS, infection, and sepsis; however, a multifactorial genesis has to be postulated.

Resuscitation with polymeric plasma substitutes is permissive for systemic inflammatory response syndrome and sepsis in multiply injured patients: a retrospective cohort study.

OBJECTIVE: Multiple trauma is often accompanied by systemic inflammatory response syndrome (SIRS). The aim of this study was to investigate the impact of polymeric plasma substitutes on the development of SIRS or sepsis. METHODS: We included 2969 patients aged ≥16 years with an Injury Severity Score (ISS) >16 in this study. The sample was subdivided into three groups: patients who did not receive colloids and those who received <5L colloids and >5L colloids within the first 48 h. Data were analyzed using IBM SPSS® for Windows version 22.0; analysis of variance was used for continuous normally distributed data and Kruskal-Wallis test for categorical data. The predictive quality of colloid treatment was analyzed using the receiver operating characteristic (ROC) curves. Independent predictively was analyzed by binary logistic regression. Data were considered significant if P < 0.05. Data are presented as the mean ± standard deviation. RESULTS: The SIRS score increased with the amount of colloid used (1.9 ± 1.4 vs. 2.4 ± 1.2 vs. 3.2 ± 0.9; P < 0.001). However, the predictive quality was low, with an area under the ROC of 0.693 for SIRS and 0.669 for sepsis (P < 0.001). Binary logistic regression revealed colloids as an independent factor for the development of SIRS and sepsis (odds ratios: SIRS 3.325 and sepsis 8.984; P < 0.001). CONCLUSION: Besides other factors, colloids have a significant permissive effect and are independent predictors for the development of SIRS and sepsis in multiply injured patients. Trial registration 'Retrospektive Analysen in der Chirurgischen Intensivmedizin' No. St. V. 01-2008.

Agraphia caused by an infarction in Exner's area.

Sigmund Exner postulated in 1881 that lesions of the base of the medial frontal gyrus could specifically produce writing impairments and attributed the writing centre to this area. We report two patients who suffered from strokes in this area. These patients suffered from writing disturbances comprising both omitted words within a sentence or badly written words, as well as aphasia. These patients, in line with prior reports, illustrate the crucial role of the Exner area at the base of the medial frontal gyrus for the cerebral writing network; we suggest that this region plays an important role for phoneme-grapheme conversions.

Obesity and overweight as a risk factor for pneumonia in polytrauma patients: a retrospective cohort study.

BACKGROUND: Obesity is a growing problem in western societies. The aim of this retrospective cohort study was to determine the association between the overweight and obese polytrauma patients and pneumonia after injury. METHODS: A total of 628 patients with an Injury Severity Score (ISS) of 16 or greater and 16 years or older were included in this retrospective study. The sample was subdivided into three groups as follows: body mass index (BMI) of less than 25 kg/m2; BMI of 25 kg/m2 to 30 kg/m2; and BMI more than 30 kg/m2. The Murray score was assessed at admission and at its maximum during hospitalization to determine pulmonary problems. Pneumonia was defined as bacteriologically positive sputum with appropriate radiologic and laboratory changes (C-reactive protein and interleukin 6). Data are given as mean ± SEM. One-way analysis of variance and the Kruskal-Wallis test were used for the analyses, and the significance level was set at p < 0.05; Bonferroni-Dunn test was performed as post hoc analysis. RESULTS: The Abbreviated Injury Scale (AIS) score for the thorax was 3.2 ± 0.1 in the group with a BMI of less than 25 kg/m2, 3.3 ± 0.1 in the group with a BMI of 25 kg/m2 to 30 kg/m2, and 2.8 ± 0.2 in the group with BMI of more than 30 kg/m2 (p = 0.044). The Murray score at admission was elevated with increasing BMI (0.8 ± 0.8 for BMI < 25 kg/m2, 0.9 ± 0.9 for BMI 25­30 kg/m2, and 1.0 ± 0.8 for BMI > 30 kg/m2; p = 0.137); the maximum Murray score during hospitalization revealed significant differences (1.2 ± 0.9 for BMI < 25 kg/m2, 1.6 ± 1.0 for BMI 25­30 kg/m2, and 1.5 ± 0.9 for BMI > 30 kg/m2; p < 0.001). The incidence of pneumonia also increased with increasing BMI (1.6% for BMI < 25 kg/m2, 2.0% for BMI 25­30 kg/m2, and 3.1% for BMI > 30 kg/m2; p = 0.044). CONCLUSION: Obesity leads to an increased incidence of pneumonia in a polytrauma situation. LEVEL OF EVIDENCE: Prognostic/epidemiologic study, level IV.

Low-dose prednisolone in addition to the initial disease-modifying antirheumatic drug in patients with early active rheumatoid arthritis reduces joint destruction and increases the remission rate: a two-year randomized trial.

OBJECTIVE: To assess the efficacy of low-dose prednisolone on joint damage and disease activity in patients with early rheumatoid arthritis (RA). METHODS: At the start of their initial treatment with a disease-modifying antirheumatic drug (DMARD), patients with early (duration < or =1 year) active RA were randomly assigned to receive either 7.5 mg/day prednisolone or no prednisolone for 2 years. Radiographs of the hands and feet were obtained at baseline and after 1 and 2 years and scored according to the Sharp score as modified by van der Heijde. Remission was defined as a Disease Activity Score in 28 joints of <2.6. Bone mineral density was measured by dual x-ray absorptiometry at baseline and after 2 years. RESULTS: Of the 250 patients included, 242 completed the study and 225 had radiographs available both at baseline and at 2 years. At 2 years, the median and interquartile range (IQR) change in total Sharp score was lower in the prednisolone group than in the no-prednisolone group (1.8 [IQR 0.5-6.0] versus 3.5 [IQR 0.5-10]; P = 0.019). In the prednisolone group, there were fewer newly eroded joints per patient after 2 years (median 0.5 [IQR 0-2] versus 1.25 [IQR 0-3.25]; P = 0.007). In the prednisolone group, 25.9% of patients had radiographic progression beyond the smallest detectable difference compared with 39.3% of patients in the no-prednisolone group (P = 0.033). At 2 years, 55.5% of patients in the prednisolone group had achieved disease remission, compared with 32.8% of patients in the no-prednisolone group (P = 0.0005). There were few adverse events that led to withdrawal. Bone loss during the 2-year study was similar in the 2 treatment groups. CONCLUSION: Prednisolone at 7.5 mg/day added to the initial DMARD retarded the progression of radiographic damage after 2 years in patients with early RA, provided a high remission rate, and was well tolerated. Therefore, the data support the use of low-dose prednisolone as an adjunct to DMARDs in early active RA.

Reduced bone mineral density in early rheumatoid arthritis is associated with radiological joint damage at baseline and after 2 years in women.

OBJECTIVE: Data suggest that reduced bone mass may be associated with radiological damage in rheumatoid arthritis (RA). We investigated if patients with reduced bone mineral density (BMD) at onset of RA had more radiological damage at onset and after 2 years than patients with normal BMD. METHODS: BMD at lumbar spine and hip was measured in 204 patients with recent RA at presentation. At baseline and after 2 years, radiographs of hands and forefeet were evaluated according to the Larsen method. At the same time-points, Disease Activity Score (DAS 28) and functional disability (the Stanford Health Assessment Questionnaire, HAQ) were assessed. RESULTS: The 134 women and 70 men had a mean age of 55 and 61 years, respectively. Reduced bone mass (RBM, Z score < or = 1.0 SD) in at least one site was found in 46.0% of women and 62.5% of men. T and Z scores correlated significantly with Larsen scores both at baseline and after 2 years for the total patient cohort. Calculated separately for the sexes, significant correlations were found only for women. Women but not men with reduced bone mass and osteoporosis had higher Larsen scores at baseline and after 2 years than those without. From a stepwise multiple logistic regression analysis Z score trochanter and baseline C-reactive protein were selected as independent predictors of joint damage, measured as proportion over the median Larsen scores. This model could explain about 25% of the "variance" in outcome (Nagelkerke R2 = 0.27). CONCLUSION: Reduced BMD at onset of RA in women was associated with a higher Larsen score at baseline and after 2 years, indicating that the development of reduced bone mass and joint destruction in RA may have a common pathophysiological mechanism.